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Query: UMLS:C0025362 (mental retardation)
 15,878 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The toxicities of many metals, such as mercury and lead, are known to man since the dawn of civilization. Organic compounds of some heavy metals are known to have a particular toxic impact on the central nervous system. Organomercury, particularly alkyl-mercuric compounds (e.g. methylmercury), has a selective effect on the granule cells of the cerebellum, the nerve cells of the calcarine cortex, and the sensory neurons in the dorsal root ganglia. The well known Minamata Bay disease is the result of a massive epidemic episode of human exposure to alkylmercury contaminated food sources. Mental retardation and other developmental defects are also known to be a consequence of exposure to this toxic metal. Organic lead compounds have been employed as gasoline additives and in other industrial purposes. Unlike its inorganic counterpart, organolead compounds have a more prominent impact on the central nervous system. Pathological changes of the brain stem neurons have been described. Organotin compounds have been used in plastic industries and as agricultural chemicals. Both trimethyl and triethyl tin compounds are found to be extremely neurotoxic. Despite the similarity of their chemical structures, trimethyl and triethyl tins have a diversely different toxic property and effects. While triethyl tin is myelinotoxic, producing edematous and vacuolar changes in the central myelin, trimethyl tin is neurotoxic, producing prominent toxic changes in the neurons of the limbic system (hippocampus, entorhinal cortex, etc.). The factors which determine the specificity and selectivity of the neurotoxic impacts by various organometals are still unknown. In view that most of the organometals are still widely employed by many countries for industrial and for agricultural purposes, caution must be made for their proper handling and disposure to avoid undesirable exposures to workers and environmental contamination of water sources and food-chain for the common public. Since organometals are difficult to eliminate from the central nervous system, injuries usually lead to permanent neurological deficits, such tragedies are frequently long lasting and create not only a medical problem, but also a social economical problem for the society.
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PMID:The neurotoxicology and pathology of organomercury, organolead, and organotin. 210 Mar 18

Both animal and vegetable life depend for their existence on appropriate amounts of various trace elements, albeit in very small amounts. This paper lists some of these trace elements and the ailments in which they play an important role. The elements discussed are gold, platinum, copper, lead, zinc, aluminium, silica, mercury, cadmium, selenium, arsenic, and iodine. The diseases involved range from multiple sclerosis, various cancers, arthritis, goitre, Down's Syndrome, and mental retardation. Less well known are Keshan, Alzheimer's, Itai-Itai, and Minamata diseases. Of particular interest in the latter part of the twentieth century is the discovery that serious deficiencies of either copper or zinc in the diet of animals may break down their immune defence mechanisms. The ability of certain plants selectively to concentrate particular heavy metals in their tissues and pollen is discussed.
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PMID:Geology, trace elements and health. 268 20

The first discovered exogenous teratogen causing mental retardation was rubella embryopathy described in 1940. Later, cytomegalic virus infection and toxoplasmosis during pregnancy and ionogenic radiation has been shown to cause embryofetopathies with concomitant mental retardation. Methyl mercury in high doses cause severe central nervous system pathology in both mothers and their fetuses. The fetal alcohol syndrome is now generally accepted as causing mostly mild mental retardation. Of therapeutic drugs, antiepileptics have been shown to carry a risk for the fetal antiepileptic syndrome complex. We have recently been able to describe fetal pathology following high intake of benzodiazepines during pregnancy.
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PMID:Prenatal factors including fetal alcohol syndrome. 289 25

An opportunity to study the effects of methylmercury poisoning in humans was provided by the large outbreak in Iraq in 1971-2. In adults, poisoning resulted from the ingestion of home-made bread prepared from methylmercury-treated seed grain and there was a highly significant correlation between the amount of bread ingested and blood mercury levels. Poisoning in infants resulted either from prior exposure in utero or from suckling or both. Blood mercury levels were higher in infants and children than in adults. There was no increased incidence of congenital defects. Symptoms and signs of poisoning and histopathological changes were mainly confined to the CNS. Symptoms developed, on average, 1-2 months after exposure. In children there was mental retardation with delayed onset of speech and impaired motor, sensory and autonomic function. Severely affected children were blind and deaf. In adults, the clinical picture could be classified as 1, mild (mainly of sensory symptoms) 2, moderate (sensory symptoms accompanied by cerebellar signs) and 3, severe (gross ataxia with marked visual and hearing loss which, in some cases, progressed to akinetic mutism followed by coma). Grades 1 and 2 carried a better prognosis thant grade 3. Interference with transmission at the myoneural junction was found in 14% of patients studied. There was no evidence of peripheral nerve involvement per se and sensory symptoms may be of central origin. The clinical differences between the Iraqi and Japanese outbreaks may be a result, in part at least, of the severe, prolonged and continuous exposure which occurred in the latter outbreak. Improvement was observed among the mild and moderate group. Treatment with chelating agents, thiol resin, haemodialysis and exchange transfusion lowered blood mercury concentrations but produced no convincing clinical benefit. To be effective, treatment may need to be instituted soon after exposure.
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PMID:Clinical and epidemiological aspects of methylmercury poisoning. 738 45

Postnatal exposure to lead or methyl mercury results in mental retardation, learning deficits, and other neurobehavioral effects in humans, and adverse consequences of prenatal exposure have been clearly documented with methyl mercury. To examine the developmental neurotoxicity of these metals, especially lead, concurrent schedules of food reinforcement were used to identify learning deficits in squirrel monkeys exposed during gestation to either methyl mercury or lead. Pregnant squirrel monkeys were administered methyl mercury (0.7 to 0.9 ppm in maternal blood) or lead (21 to 79 micrograms/dl in maternal blood) during the last half to two-thirds of gestation. At about 5-6 years of age, offspring were trained to lever press under concurrent schedules of reinforcement in which separate random interval reinforcement schedules operated independently on two levers. Reinforcement densities were varied such that 20 to 90% of the reinforcers were programmed to derive from the left lever (i.e., one lever was "richer" than the other). At steady state, the behavior of the controls was sensitive to reinforcement density and showed little lever bias, but the behavior of monkeys exposed to more than 40 micrograms/dl of lead and to methyl mercury was less sensitive to reinforcement rates and heavily biased. When relative reinforcement density on a lever changed, the unexposed animals' response rates gradually shifted to the newly rich lever. The behavior of monkeys exposed to methyl mercury or more than 40 micrograms/dl of lead changed slowly, not at all, or in the wrong direction. Steady-state behavior of monkeys exposed to less than 40 micrograms/dl resembled controls, but acquisition progressed more slowly and required 2-4 times as many reinforcers to complete. These effects suggest a behavioral mechanism--insensitivity to changing reinforcement contingencies--by which learning deficits and behavioral changes associated with these metals might be related to toxicant exposure. Since maternal blood levels corresponded to those that could be experienced in occupational settings, the present data raise the possibility of fetal hazards associated with maternal lead exposures at levels tolerated in humans in occupational settings.
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PMID:Prolonged behavioral effects of in utero exposure to lead or methyl mercury: reduced sensitivity to changes in reinforcement contingencies during behavioral transitions and in steady state. 818 34

In a case-referent study on mental retardation and parental occupation, the applicability of job exposure matrices for the identification of risk factors was evaluated. The parents of 306 mentally retarded children (cases) and 322 referents were interviewed about their occupational activities in the pregnancy period. Detailed occupational histories were obtained that were compared with exposures generated by two different job exposure matrices. The agreement between interview and matrices was low: the sensitivity ranged from 17.9% to 32.4% and the percentages of false positive exposures from 66.7% to 96.0%. By means of the interview, significantly increased odds ratios (ORs) were found for exposure of the mother in late pregnancy to radiation (OR = 9.3), mercury (OR = 8.7), organic solvents (OR = 1.7), hair cosmetics and dyes (OR = 3.7), paint (OR = 2.7), hexachlorophene/phenylphenol (OR = 3.1), antibiotics (OR = 2.9), and dust (OR = 2.2) and for working with copying machines (OR = 3.0) or in occupations with poor climatological circumstances and permanent contact with people. The last was confirmed by the British matrix (OR = 1.7). Otherwise, most of the mentioned associations were missed by the job exposure matrices. Therefore, these matrices were not considered to be applicable in this particular study, nor in most other reproductive epidemiological studies in view of their general properties and limitations.
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PMID:Mental retardation and parental occupation: a study on the applicability of job exposure matrices. 795 1

The methylmercury exposure of patients with congenital or infantile Minamata disease is known only from a small number of analyses of umbilical cords. Four laboratories in Japan have analyzed a total of 176 samples of umbilical cord tissue obtained from Minamata. The highest concentrations were seen in cord tissue from children born during 1950-1965, i.e., the peak period of acetaldehyde production in Minamata before installation of waste water treatment. Twenty-four samples from patients diagnosed with Minamata disease showed a median mercury concentration of 1.63 microg/g and differed significantly from levels seen in cord tissue from control children. However, children diagnosed with mental retardation had mercury concentrations in cord that were intermediate between the two other groups. Using regression coefficients obtained at a study conducted at the Faroe Islands, the median cord mercury concentration from the children with Minamata disease is estimated to correspond to about 216 microg/L cord blood and 41 microg/g in maternal hair. Based on correlations reported in the literature, the median daily mercury intake of the women whose children developed Minamata disease can then be estimated at about 225 microg. Although these children had fully developed Minamata disease, the estimates of median mercury levels are only four to five times higher than current mercury exposure limits.
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PMID:Methylmercury dose estimation from umbilical cord concentrations in patients with Minamata disease. 960 Aug 2

Mercury is present in the earth's crust and is methylated by bacteria in aquatic environments to methylmercury (MeHg). It is then concentrated by the food chain so predatory fish and sea mammals have the highest levels. Thus, consuming seafood leads to exposure. MeHg readily crosses the placenta and the blood-brain barrier and is neurotoxic. The developing fetal nervous system is especially sensitive to its effects. Prenatal poisoning with high dose MeHg causes mental retardation and cerebral palsy. Lower level exposures from maternal consumption of a fish diet have not been consistently associated with adverse neurodevelopmental outcomes. However, most studies have considerable uncertainty associated with their results. Two large controlled longitudinal studies of populations consuming seafood are underway that are likely to determine if any adverse effects can be identified. No adverse associations have been found in the Seychelles, where exposure is mainly from fish consumption. In the Faroe Islands where exposure is primarily from consumption of whale meat and not fish, adverse associations have been reported. The Seychelles population consumes large amounts of marine fish containing MeHg concentrations similar to commercial fish in the United States. Current evidence does not support the hypothesis that consumption of such fish during pregnancy places the fetus at increased neurodevelopmental risk.
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PMID:Prenatal methylmercury exposure and children: neurologic, developmental, and behavioral research. 964 47

Methylmercury (MeHg) is a potent neurotoxin that in high exposures can cause mental retardation, cerebral palsy, and seizures. The developing brain appears particularly sensitive to MeHg. Exposure levels in pregnant experimental animals that do not result in detectable signs or symptoms in the mother can adversely affect the offspring's development. Studies of human poisonings suggest this may also occur in humans. Human exposure to MeHg is primarily dietary through the consumption of fish: MeHg is present in all fresh and saltwater fish. Populations that depend on fish as a major source of dietary protein may achieve MeHg exposure levels hypothesized to adversely affect brain development. Increasing mercury levels in the environment have heightened concerns about dietary exposure and a possible role for MeHg in developmental disabilities. Follow-up studies of an outbreak of MeHg poisoning in Iraq revealed a dose-response relationship for prenatal MeHg exposure. That relationship suggested that prenatal exposure as low as 10 ppm (measured in maternal hair growing during pregnancy) could adversely affect fetal brain development. However, using the same end points as were used in the Iraq study, no associations have been reported in fish-eating populations. Using a more extensive range of developmental end points, some studies of populations consuming seafood have reported associations with prenatal MeHg exposure, whereas others have found none. This paper reviews the data presently available associating MeHg exposure with development and poses some of the unanswered questions in this field.
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PMID:Does methylmercury have a role in causing developmental disabilities in children? 1085 38

Perinatal exposure to methylmercury is known to result in severe neurological effects on the developing fetus and infant, including cerebral palsy, mental retardation, and seizures. Males are more susceptible than females to neurological damage from perinatal methylmercury exposures. Preliminary analyses of data and statistics for the hospitalization rates of males for cerebral palsy in the 17 Canadian Areas of Concern in the Great Lakes basin indicate a possible geographic association with locations with elevated mercury from natural or industrial sources.
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PMID:Male cerebral palsy hospitalization as a potential indicator of neurological effects of methylmercury exposure in Great Lakes communities. 1522 71


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