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Results for “Lead Poisoning, Nervous System”

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At least 19 recordsLinked to original sources
PubMed2001

Exposure to lead appears to selectively alter metabolism of cortical gray matter.

OBJECTIVE: The effects of lead poisoning on the development of children have been examined primarily in the context of behavioral and neuropsychological studies. The purpose of this study was to examine the in vivo use of magnetic resonance spectroscopy (MRS) for the evaluation of the neurotoxic effects of lead on the nervous system. MRS has the ability to monitor brain metabolism by detecting a number of neurochemicals among which is N-acetylaspartate, a metabolite shown to decrease in processes that involve neuronal loss. METHODS: In the present study we evaluated the metabolism of gray and white matter of frontal cortex using MRS in individuals with elevated blood lead levels and compared the results with those obtained on nonlead-exposed controls. RESULTS: Although all of the participants had normal MRI examinations of the brain, the lead-exposed individuals exhibited a significant reduction in the N-acetylaspartate/creatine and phosphocreatine ratios in frontal gray matter compared with the nonlead-exposed controls. CONCLUSIONS: The findings of this study suggest that lead has an effect on brain metabolites as detected by MRS in vivo. More specifically, we have found statistically significant reduced levels of brain metabolites in gray but not white matter in lead-exposed individuals. These results imply that MRS is able to detect metabolic abnormalities in individuals with lead poisoning.

Adolescent↗
PubMed2005

Lead neurotoxicity: from exposure to molecular effects.

The effects of lead (Pb(2+)) on human health have been recognized since antiquity. However, it was not until the 1970s that seminal epidemiological studies provided evidence on the effects of Pb(2+) intoxication on cognitive function in children. During the last two decades, advances in behavioral, cellular and molecular neuroscience have provided the necessary experimental tools to begin deciphering the many and complex effects of Pb(2+) on neuronal processes and cell types that are essential for synaptic plasticity and learning and memory in the mammalian brain. In this review, we concentrate our efforts on the effects of Pb(2+) on glutamatergic synapses and specifically on the accumulating evidence that the N-methyl-D-aspartate type of excitatory amino acid receptor (NMDAR) is a direct target for Pb(2+) effects in the brain. Our working hypothesis is that disruption of the ontogenetically defined pattern of NMDAR subunit expression and NMDAR-mediated calcium signaling in glutamatergic synapses is a principal mechanism for Pb(2+)-induced deficits in synaptic plasticity and in learning and memory documented in animal models of Pb(2+) neurotoxicity. We provide an introductory overview of the magnitude of the problem of Pb(2+) exposure to bring forth the reality that childhood Pb(2+) intoxication remains a major public health problem not only in the United States but worldwide. Finally, the latest research offers some hope that the devastating effects of childhood Pb(2+) intoxication in a child's ability to learn may be reversible if the appropriate stimulatory environment is provided.

Animals↗
PubMed2005

The relationship between lead exposure, motor function and behaviour in Inuit preschool children.

The main focus of this study was to determine the role of behaviour in the relationship between postnatal lead exposure and motor function. The sample consisted of 110 preschoolers, of age 5, from Nunavik. Lead concentration was measured at birth and at testing time. Average lead levels were of 4.9 microg/dL (0.24 micromol/L) and 5.3 microg/dL (0.26 micromol/L) for cord and child blood, respectively. Children's balance and fine motor capacities were tested. A modified version of the IBR was used to assess behaviour. Postnatal blood lead concentrations correlated positively with both impulsivity and activity. Neither pre- nor postnatal blood lead concentration correlated with attention level. The children's scores on impulsivity (I) and activity (A) were summed to create the independent variable IA, which was tested as a potential mediator between lead exposure and two dependent variables: the coefficient of covariation in alternating hand movements and transversal sway in tandem position. Mediation was significant only for the latter variable. IA and attention were then tested as potential moderators in the relation between postnatal lead exposure and motor function. No significant interaction between independent variables could be observed. These results do not support the hypothesis that, at low levels of postnatal exposure, lead acts indirectly on motor function via behaviour. However, IA does act as a mediator in the relationship between postnatal blood lead concentration and transversal sway in tandem position.

Adult↗
PubMed2002

Maternal bone lead as an independent risk factor for fetal neurotoxicity: a prospective study.

OBJECTIVE: A number of prospective studies have examined lead levels in umbilical cord blood at birth as predictors of infant mental development. Although several have found significant inverse associations, others have not. Measurement of lead levels in maternal bone, now recognized as the source of much fetal exposure, has the potential to serve as a better or complementary predictor of lead's effect on the fetus. Our objective was to compare lead levels in umbilical cord blood and maternal bone as independent predictors of infant mental development using a prospective design. METHODS: We recruited women who were giving birth at 3 maternity hospitals in Mexico City that serve a homogeneous middle-class community. Umbilical cord blood lead levels were measured by graphite furnace atomic absorption spectroscopy, and maternal lead levels in cortical (tibial) and trabecular (patellar) bone were measured within 4 weeks of giving birth using a 109-Cd K-x-ray fluorescence instrument. At 24 months of age, each infant was assessed using the Bayley Scales of Infant Development-II (Spanish Version). RESULTS: A total of 197 mother-infant pairs completed this portion of the study and had data on all variables of interest. After adjustment for other well-known determinants of infant neurodevelopment, including maternal age, IQ, and education; paternal education; marital status; breastfeeding duration; infant gender; and infant illness, lead levels in umbilical cord blood and trabecular bone were significantly, independently, and inversely associated with the Mental Development Index (MDI) scores of the Bayley Scale. In relation to the lowest quartile of trabecular bone lead, the second, third, and fourth quartiles were associated with 5.4-, 7.2-, and 6.5-point decrements in adjusted MDI scores. A 2-fold increase in cord blood lead level (eg, from 5 to 10 micro g/dL) was associated with a 3.1-point decrement in MDI score, which is comparable to the magnitude of effect seen in previous studies. CONCLUSION: Higher maternal trabecular bone lead levels constitute an independent risk factor for impaired mental development in infants at 24 months of age. This effect is probably attributable to mobilization of maternal bone lead stores, a phenomenon that may constitute a significant public health problem in view of the long residence time of lead in bone.

Bone and Bones↗
PubMed1990

[Morphological changes in the nervous system in lead poisoning. I. Experimentally induced lead neuropathy].

A morphological study on experimental model of lead (Pb) neuropathy (by the method of Pentschev, A., 1966) was described. Dense inclusions in Schwann's cells and satellite cells of the sensory ganglia were found by an electron microscope in the examined peripheral nerves (n. ischiadicus) and sensory ganglia (g. lumbale and g. trigeminale--Gasseri). These finding supported direct toxic action of Pb on these structures and proved their participation in the pathogenesis of developing neuropathy.

Animals↗
PubMed1993

[Morphological changes in the nervous system in lead poisoning. II. Experimental lead-induced encephalopathy].

The morphological investigation in an experimental model of lead (Pb) encephalopathy (according to the method of A. Pentschew, 1966) is presented. Electron microscopy-dense inclusions are found out in the nuclei and cytoplasm of astrocytes and in some ependyma cells in the investigated cortical and subcortical (paraventricular) structure of the brain and spinal cord. This confirms the direct toxic action of Pb on these structures and proves their participation in pathogeneses of the developing encephalopathy. The established inclusions in the ependyma and the data about a disturbance of the blood-brain barrier give a reason to be proposed the possibility for a penetration of Pb in the nervous system not only through a blood but also through a cerebrospinal fluid way.

Animals↗
PubMed1999

Distortion product oto-acoustic emissions in Andean children and adults with chronic lead intoxication.

Neuroauditory disorders and sensory-neural hearing loss have been suggested as possible etiologic factors in the neurodevelopmental learning disabilities attributed to lead (Pb) intoxication. However, studies relating hearing loss to Pb poisoning have presented disparate results, suggesting that auditory sensitivity may not be a reliable marker of Pb intoxication. Oto-acoustic emissions, sounds that can be recorded non-invasively from the ear canal and are preneural responses of the outer hair cells of the inner ear, have been found to be diminished in ears exposed to some toxic agents. In the current study, distortion product oto-acoustic emissions (DPOAEs) were obtained from 28 ears of 14 children and 10 ears of 5 adults living in a highly Pb-contaminated environment in remote villages in the Andes Mountains of Ecuador. Blood lead (PbB) levels for the children (ages: 5-14 years) ranged from 33.4 to 118.2 microg/dl (mean: 51.5; SD: 22.9 microg/dl), or 3-12 times higher than the U.S. Centers for Disease Control and Prevention's toxic level of 10 microg/dl. The PbB levels for the adults ranged from 19.2 to 55.7 microg/dl. Despite the high PbB levels, the children had normal hearing thresholds, and DPOAEs were present for the children at the following f2 frequencies: 1187, 1500, 1906, 2406, 3031, 3812, 4812 and 6031 Hz. Although there was a tendency for the children to have diminished DPOAEs, no consistent correlation of DPOAEs with PbB level was found. The adults had diminished DPOAEs that were consistent with their observed, probably noise-related hearing loss. Contrary to some reports in the literature, the current results show no unequivocal clinical or subclinical evidence that high PbB levels have a toxic effect on the cochlea.

Adolescent↗
PubMed2004

Lead poisoning.

Understanding of lead toxicity has advanced substantially over the past three decades, and focus has shifted from high-dose effects in clinically symptomatic individuals to the consequences of exposure at lower doses that cause no symptoms, particularly in children and fetuses. The availability of more sensitive analytic methods has made it possible to measure lead at much lower concentrations. This advance, along with more refined epidemiological techniques and better outcome measures, has lowered the least observable effect level until it approaches zero. As a consequence, the segment of the population who are diagnosed with exposure to toxic levels has expanded. At the same time, environmental efforts, most importantly the removal of lead from gasoline, have dramatically reduced the amount of lead in the biosphere. The remaining major source of lead is older housing stock. Although the cost of lead paint abatement is measured in billions of dollars, the monetized benefits of such a Herculean task have been shown to far outweigh the costs.

Adolescent↗