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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From March 1974-July 1975, 76 (57%) of 133 persons who had worked at a pesticide plant that produced Kepone, a chlorinated hydrocarbon insecticide, contracted a previously unrecognized clinical illness characterized by nervousness, tremor, weight loss, opsoclonus, pleuritic and joint pain, and oligospermia. Illness incidence rates for production workers (64%) were significantly higher than for nonproduction personnel (16%). The mean blood Kepone level for workers with illness was 2.53 ppm and for those without disease 0.60 ppm (p0.001). Blood Kepone levels in current workers (mean, 3.12 ppm) were higher than those in former employees (1.22 ppm). Blood Kepone levels for workers in nearby businesses and for residents of a community within 1.6 km of the plant ranged from undetectable to 32.5 ppb. Illness attributable to Kepone was found in wives of 2 Kepone workers; there was no apparent association between frequency of symptoms and proximity to the plant in the survey of the community population.
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PMID:Epidemic kepone poisoning in chemical workers. 7 69

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.
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PMID:Chlordecone intoxication in man. I. Clinical observations. 7 55

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.
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PMID:Chlordecone intoxication in man. II. Ultrastructure of peripheral nerves and skeletal muscle. 7 56

The effects of the chlorinated pesticide chlordecone on food intake, body weight, and water intake were examined in adult male rats. Chlordecone treatment produced a dose dependent suppression of food intake. Loss of body weight accompanied the reduced food intake. However, chlordecone did not suppress water intake. Chlordecone treated animals maintained on a liquid diet also demonstrated reduced food intake, suggesting that chlordecone has a specific effect on feeding behavior and not a general effect on ingestive behaviors. The potential contribution of chlordecone-induced tremor to the suppressed food intake and the loss of body weight was considered. When treatment occurred immediately before a 24 hr fast, controls and animals given 75 mg/kg showed no differences in the body weight decline, even though tremor occurred in the pesticide-treated rats. Thus, it is unlikely that tremor alone produced the body weight loss observed in the present experiment. Similarly, animals were capable of initiating eating behavior even though tremor was present. In addition, chlordecone treatment inhibited food intake within 2 hr. Consequently, these results suggest that chlordecone suppresses food intake which in turn produces the decline in body weight.
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PMID:Effects of chlordecone on food intake and body weight in the male rat. 127 91

The effect of the estrogen-like chlorinated pesticide chlordecone (Kepone) on sexual behavior was examined in proestrous rats following treatment with 25, 50, or 75 mg/kg chlordecone. In most animals, sexual behavior, both receptivity and proceptivity, was reduced within 60 min following the higher dosage of chlordecone. Reduced sexual receptivity occurred more slowly with 50 mg/kg chlordecone (usually within 180 min) and no reduction was seen following 25 mg/kg chlordecone. The reduced sexual behavior after chlordecone treatment preceded the onset of marked chlordecone-induced tremor. A group of rats treated with 75 mg/kg chlordecone was euthanized at the time that behavioral inhibition began to develop. The content of serotonin, norepinephrine, and their principal metabolites was determined by high-performance liquid chromatography of extracts of brain tissue of these animals. In hypothalamus, increases in serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) content, and a decrease in the level of norepinephrine (NE), were detected in chlordecone-treated rats relative to matched controls which received vehicle. The content of 5-HT was also increased in preoptic area of chlordecone-treated females. The content of the catecholamine metabolite, 3,4-dihydroxy-phenylacetic acid, was unaffected by chlordecone in either part of brain. These are the first observations of the parallel effects of chlordecone on receptive and proceptive behaviors, and on neurochemistry, in female rats; the results demonstrate short-latency effects of the pesticide treatment on the CNS events that mediate female reproductive behavior. Results of previous studies had led to the suggestion that chlordecone's inhibition of sexual behaviors resulted from its interaction with the intracellular estrogen receptor. However, the rapidity of the inhibition during the period of ongoing sexual behavior makes it unlikely that the inhibition is mediated by the pesticide's action at the intracellular estrogen receptor. Because of the importance of sexual behaviors to reproductive fitness, the current results indicate that nonsteroidal, behavioral mechanisms could contribute to chlordecone's neuroreproductive toxicity.
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PMID:Chlordecone (Kepone) on the night of proestrus inhibits female sexual behavior in CDF-344 rats. 171 37

Chlordecone (0.1 to 10 mg) or corn oil vehicle was injected into Japanese quail eggs on day 1 of incubation. Higher doses (0.5-10 mg per egg) produced tremor and ataxia at hatching and dose-related decreases in hatchability and survivability. Doses lower than 0.25 mg per egg had no effects. Gonad weights were not affected at 12 weeks of age. A second study examined the effect of injecting 0.5 mg of chlordecone into the egg on day 1, 3, 7 or 14 of incubation. Chlordecone-induced tremor was present at hatching regardless of the day of injection. Significant decreases in hatchability and increases in embryonic mortality were seen when chlordecone was injected on day 1 of incubation. Survivability to 5 weeks of age was decreased in birds receiving chlordecone on day 1 or 3 of incubation. At 75 to 84 days of age, egg production was decreased only in birds injected on day 1 of incubation. The offspring from these studies were mated and the hatchability and reproductive capability of these birds was studied at 75 to 84 days of age and found to be not significantly affected. In a third study, birds exposed to 0.5 mg of chlordecone or vehicle on day 1 of incubation were trained as adults in a food reinforced operant task. Exposure to chlordecone affected performance during the first 3 of 15 days of a match-to-sample task. The baseline response rate of these animals on a food reinforced random interval 60 sec schedule was then determined. During the last two weeks of asymptotic performance, chlordecone-exposed birds had a significantly lower rate of responding than controls. These data indicate that in ovo exposure to chlordecone can have significant long-term effects on conditioned behavior and egg production, particularly if exposure occurs on day 1 of incubation.
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PMID:Direct administration of chlordecone into Japanese quail eggs has persistent effects on conditioned behavior of adults. 243 60

Occupational exposures to neurotoxic chemicals have produced large outbreaks of illness in chemical and pesticide workers worldwide. Outbreaks of occupational neurologic disease in the United States have included (1) the Kepone episode in Hopewell, Virginia, in which 76 workers at a pesticide plant producing the chlorinated hydrocarbon insecticide, Kepone, developed a previously unrecognized syndrome of nervousness, tremor, ataxia, weight loss, opsoclonus, pleuritic and joint pain, and oligospermia; (2) an outbreak of 104 cases of autonomic neuropathy in polyurethane foam workers in Marblehead, Massachusetts, manifest principally by urinary bladder dysfunction, which followed exposure to a new catalyst, dimethylaminopropionitrile (DMAPN); and (3) an outbreak of acute mixed motor and sensory neuropathy in 48 plastic fabric workers in Columbus, Ohio, exposed to the solvent methyl butyl ketone (MBK). These outbreaks underscore the vulnerability of chemical workers to neurotoxins. In addition, occurrence of these large, easily detectable epidemics suggests that many more smaller clusters and single cases of neurologic disease of undetermined origin, particularly in younger adults, may be caused by exposure to occupational or to other toxic chemicals. Detection of the etiology of chemically induced neurologic illness requires a high index of suspicion and careful ascertainment of occupational history.
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PMID:Clinical epidemiology of occupational neurotoxic disease. 616 Apr 6

Chlordecone or Kepone is a polycyclic chlorinated hydrocarbon insecticide that produces hyperexcitability, tremor, and other signs of nervous system toxicity. In addition, chlordecone has estrogenic-like effects and disturbs neuroendocrine function. Studies at the neurochemical level indicate that chlordecone inhibits neurotransmitter uptake; steady-state levels of biogenic amines are generally resistant to chlordecone, especially in mice. At the subcellular level, chlordecone may destabilize membrane function by altering energy metabolism and/or the disposition of ions required for neural transmission.
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PMID:Chlordecone neurotoxicity: a brief overview. 618 53

Chlordecone is an organochlorine insecticide which intoxicated a number of workers in 1975 because of excessive exposure in the industrial plant. The major manifestations were tremor, opsoclonus, arthralgias, pleural pain, and reduced sperm count. The half-life in blood was determined to be 165 days, but treatment with cholestyramine reduced this to 80 days. Despite initial high blood levels of chlordecone, follow up at six years indicated that in the workers reevaluated the chlordecone had been cleared completely from blood, with very low levels remaining in fat. As the chlordecone was cleared, the clinical manifestations abated, and many of the patients returned to work. Appropriate industrial hygienic and medical management would probably have quickly aborted the epidemic.
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PMID:Neurological manifestations in humans exposed to chlordecone and follow-up results. 618 68