Lead, mental health, and social action: a view from the bridge.
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Results for “Lead Poisoning, Nervous System, Adult”
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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.
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[Saturnism: an emergency plan].
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Emergencies↗
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.
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[Diagnostic problems in case of environmental exposure to tetraethyl lead].
UNLABELLED: The aim of this study was the presentation of the chronic tetraethyl lead poisoning of the 4 person family in the place of settlement. CASE REPORT: 15.5-years-old man was admitted to the regional Pediatric Ward because of changes of behavior, hallucinations, agitation. Nausea, vomiting, metallic taste and diarrhea were observed prior to the admission. In the case history, there were no data suggested of the toxic origin of the disorder . The CSF examination and CT of the brain were normal. Increased activity of CPK, ALT, AST, GTP, LDH in the blood were found. Paranoid syndrome was diagnosed by psychiatric evaluation. The patients' mother presented similar signs in almost the same time. The laboratory tests of the blood taken from the patients' father and older brother revealed the increase activity of the same enzymes (CPK, ALT, AST, LDH). All family was admitted to the Department of Clinical Toxicology in Kraków because of suspicion of the heavy metal poisoning. The toxicological laboratory test showed in all described patients the toxic serum lead concentration accordingly: 440 microg/l--older brother, 490 microg/l--father, 508 microg/l--mother and 635 microg/l--primary described patient. Because of the fact, that were no characteristic for lead poisoning changes in blood picture, the toxicological investigations were continued. As a result of these examinations presence of a diethyl lead in urine was confirmed. In the evaluation of the multiorgan damages connected with tetraethyl lead poisoning, we paid special attention on CSN dysfunctions. The USG and scintigraphy examinations revealed the liver damage. The different kinds of arrhythmias indicated on cardiovascular system damage. Based on clinical presentation and laboratory investigations the chronic tetraethyl lead poisoning was diagnosed.
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[Late sequelae of tetraethyl lead poisoning].
In our previous study a tetraethyl lead poisoning due to a rural environmental exposure of four family members was described. A differently intensified OUN dysfunction dominated clinical picture. Cognition status and degree of OUN dysfunction was monitored using generally accepted neurobehavioral test battery. The tests applied were fitted individually to each poisoned family member in accordance to current intensification of symptoms. Basing on the neurobehavioral performance results a consecutive imagine techniques were introduced to full CNS evaluation of intoxicated patients. Results of neuropsychological monitoring in 12 months period were compared to brain CT, SPET 99mTc-ECD used to evaluation of regional brain perfusion disturbances, MRI and MRS and presented in the study.
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A meta-analysis for neurobehavioural results due to occupational lead exposure with blood lead concentrations <70 microg/100 ml.
The size of performance effects caused by exposure to inorganic lead was determined by a meta-analytical procedure. Twenty-two studies covering exposure conditions of <70 microg/100 ml blood lead concentration were considered as to whether the methods of recording performance deficits were comparable. As a consequence of different test procedures and insufficient documented test results only 13 tests out of 12 studies could be included in the analysis. For the tests Block Design, Logical Memory and Santa Ana performance deficits were found, which may be interpreted as 'small' effects in accordance with a convention for evaluating effect sizes. For the example of Block Design it could be shown that these effects are nevertheless serious. The extent of the exposure related decrease of performance was comparable with those changes of performance which can be expected during aging of up to 20 years. Subsequently, a blood lead concentration of 70 microg/100 ml cannot be considered as a safe limit against long-term decreases of psychological performance.
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The relationship between blood lead levels and neurobehavioral test performance in NHANES III and related occupational studies.
OBJECTIVES: The goals of this study were two-fold: (1) to assess the relationship between blood lead levels and neurobehavioral test performance in a nationally sample of adults from the third National Health and Nutrition Evaluation Survey and (2) to analyze the results from previously published studies of occupational lead exposure that used the same neurobehavioral tests as those included in the survey. METHODS: Regression models were used to test and estimate the relationships between measurements of blood lead and performance on a simple reaction time, a symbol-digit substitution, and a serial digit learning test in adults aged 20-59 years who participated the survey. Mixed models were used to analyze the data from the occupational studies. RESULTS: The blood lead levels of those participating in the survey ranged from 0.7 to 41.8 microg/dl. The estimated geometric mean was 2.51 microg/dl, and the estimated arithmetic mean was 3.30 microg/dl. In the survey, no statistically significant relationships were found between blood lead concentration and performance on the three neurobehavioral tests when adjusted for covariates. In the occupational studies, the groups exposed to lead consistently performed worse than control groups on the simple reaction time and digit-symbol substitution tests. CONCLUSIONS: The results from the survey and the occupational studies do not provide evidence for impairment of neurobehavioral test performance at levels below 25 microg/dl, the concentration that the Centers for Disease Control and Prevention define as elevated in adults. The average blood lead level of the exposed groups in the occupational studies was 41.07 microg/dl, less than 50 microg/dl, the minimum concentration that the Occupational Safety and Health Administration requires for medical removal from the workplace. Given the evidence of impaired neurobehavioral performance in these groups, the 50 microg/dl limit should be reevaluated.
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Lead encephalopathy: CT and MR findings.
Lead is toxic to many organ systems, among them bone marrow, muscles, kidneys, endocrine glands, joints, and nervous system. Encephalopathy is a rare but severe complication of lead poisoning. Lead toxicity is much less common in adults. Adult lead poisoning results primarily from exposure by inhalation in the workplace. In this report, two cases of adult toxic encephalopathy due to lead poisoning are presented with CT and MR findings.
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Pre- and posttreatment MR imaging findings in lead encephalopathy.
A 41-year-old man suspected of having lead poisoning was evaluated with MR imaging before and after British antilewisite therapy. The MR imaging findings showed bilateral symmetric involvement of the occipital lobe, affecting predominantly the gray-white matter junction and the subcortical white matter. A right cerebellar lesion was noted, with focal hyperintensities involving the gray-white matter. Similar lesions were seen in the temporal, parietal, and frontal regions. These lesions resolved after chelation therapy.
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Occupational lead exposure and longitudinal decline in neurobehavioral test scores.
BACKGROUND: No previous longitudinal studies have compared and contrasted associations of blood lead and tibia lead with declines in cognitive function over the course of time in a large sample of subjects with current and past occupational exposure to inorganic lead. METHODS: From 1997 through 2001, we conducted a longitudinal study of 803 current and former lead workers in South Korea to evaluate effects on the central and peripheral nervous systems. Three study visits occurred during a mean follow-up duration of 2.20 years. Neurobehavioral test scores, peripheral nervous system function, and blood lead were measured at each of the 3 study visits, whereas tibia lead was measured by x-ray fluorescence at the first and second visits. We limited our analysis to the 576 lead workers who completed testing at all 3 visits. We performed regression analyses using generalized estimating equations. RESULTS: There were consistent associations of blood lead with test scores at baseline and of tibia lead with declines in test scores over the next year, mainly in executive abilities, manual dexterity, and peripheral vibration threshold. CONCLUSIONS: The results support the inference that occupational lead exposure can cause declines in cognitive function over the course of time. Lead likely has an acute effect on neurobehavioral test scores as a function of recent dose and a longer-term (possibly progressive) effect on cognitive decline as a function of cumulative dose.
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Differential effects of lead exposure on components of verbal memory.
AIMS: To determine if verbal learning and memory requiring acquisition and retention of information is differentially affected by lead exposure. METHODS: The Rey Auditory Verbal Learning Test (RAVLT), a test of verbal learning and memory, was administered to 256 English speaking lead smelter workers who had a mean (SD) age of 41 (9.4) years and employment duration of 17 (8.1) years. Lead exposure variables, based on up to 25 years of prior blood lead data, included a mean (SD) current blood lead (PbB) of 28 (8.8) microg/dl, working lifetime time weighted average blood lead (TWA) of 39 (12.3) microg/dl, and working lifetime integrated blood lead index (IBL) of 728 (434.4) microg-y/dl. Associations of these chronic and recent lead exposure variables with measures from the RAVLT were modelled through multiple linear regressions after controlling for age and educational achievement. RESULTS: PbB was not associated with any of the RAVLT variables. However, TWA and IBL contributed significantly to the explanation of variance of measures of encoding/storage and retrieval but not to immediate memory span, attention, and learning. Grouping study participants by RAVLT performance according to three recognised clinical memory paradigms showed significantly higher TWA and IBL in the group with "generalised memory impairment" after adjusting for age and educational achievement. We examined recall mechanisms in each group by serial position in the word list and found stronger primacy (recall of words from the beginning of the list) in the "no impairment" and "retrieval difficulties" groups while the "generalised memory impairment" group had better performance on recency (recall of words from the end of the list). CONCLUSIONS: Lead exposure over years and not PbB interfered with the organisation and recall of previously learned verbal material. Chronic lead exposure affects encoding/storage and retrieval of verbal information.
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Ayurvedic medicine: patients in peril from plumbism.
Heavy metals are commonly incorporated into Ayurvedic preparations as ashes or 'bhasmas'. A widely disseminated belief within Ayurvedic medicine is that these heavy metals can be valuable therapeutic components. Western toxicology refutes this contention. We report eight cases of lead poisoning occurring in or near the Auckland region of New Zealand. In all cases, poisoning was attributable to consumption of Ayurvedic 'herbal medicines'. Whole blood lead levels ranged from 1.5 to 6.9 micromol/L. Six patients had symptomatic lead poisoning, requiring treatment with chelation therapy. A high index of suspicion is required to detect lead poisoning, which should be suspected in people taking Ayurvedic remedies, especially if they have associated anaemia or abdominal symptoms.
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Comparison of patella lead with blood lead and tibia lead and their associations with neurobehavioral test scores.
OBJECTIVE: Lead exposure in adults is associated with worse cognitive function in cross-sectional and longitudinal studies. Previous studies have mainly examined relations with blood lead or cortical bone lead; few have examined trabecular bone lead. METHODS: We performed a cross-sectional analysis of the relations of patella lead and other lead biomarkers with measures of neurobehavioral and peripheral nervous system function in 652 lead workers. RESULTS: Patella lead was found to be associated with worse performance on seven of 19 tests of manual dexterity, sensory vibration threshold, and depressive symptoms. The associations of patella lead with cognitive function were essentially similar to those with blood lead or tibia lead but of somewhat lower magnitude. CONCLUSIONS: In this study, measurement of patella lead did not aid causal inference regarding cognitive effects when compared with blood lead and tibia lead.
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Reduced cognitive abilities in lead-exposed men.
OBJECTIVES: Since it is still controversial whether-low-to moderate long-term lead exposure below current threshold values causes neurobehavioural deficits in adults, we investigated executive functions of the prefrontal cortex, attention, and visuospatial and visuomotor functioning in lead-exposed subjects. METHODS: Forty-seven lead-exposed subjects with a mean blood lead (PbB) level of 30.8 microg/100 ml and 53 non-lead-exposed aged-matched subjects (PbB: 4.32 microg/100 ml) with the same socio-economic background were investigated. Both groups were also matched on verbal intelligence. Neuropsychological tests were done by the modified Wisconsin card sorting test, block design test, visual recognition test, simple reaction time, choice reaction and digit symbol substitution. Lead exposure was assessed by current and cumulative measures. RESULTS: While there were significant differences in the results of the Wisconsin, block design and visual recognition tests, no differences were found in simple reaction time, choice reaction and digit symbol substitution. Significant correlations existed between current exposure and cognitive deficits. No correlation was found between cumulative exposure measures and cognitive parameters. CONCLUSIONS: Our results show that PbB below 70 microg/100 ml reduce neurobehavioural abilities, particularly visuospatial abilities and executive functions referring to the prefrontal cortex. As neurobiological substrate of the prefrontal dysfunction, glutamatergic system disturbances are discussed.
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Metal exposure and common chronic diseases: a guide for the clinician.
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Active and passive smoking and blood lead levels in U.S. adults: data from the Third National Health and Nutrition Examination Survey.
Lead is a component of tobacco and tobacco smoke. We examined the relationship between current, former, and passive smoking and blood lead levels in a nationally representative sample of 16,458 U.S. adults, aged 17 years or older, who participated in the Third National Health and Nutrition Examination Survey (1988-1994). We used linear and logistic regression modeling, adjusting for known covariates, to determine the relationship between smoking and blood lead levels. Geometric mean blood lead levels were 1.8 microg/dl, 2.1 microg/dl, and 2.3 microg/dl in never-smokers with no, low, and high cotinine levels, respectively. Levels were 2.9 microg/dl in former smokers and 3.5 microg/dl in current smokers. The adjusted linear regression model showed that geometric mean blood lead levels were 30% higher (95% CI = 24%-36%) in adults with high cotinine levels than they were in those with no detectable cotinine. Active and passive smoking is associated with increased blood lead levels in U.S. adults.
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Assessment of neurobehavioral performance as a function of current and cumulative occupational lead exposure.
A cross sectional field study was planned to assess neurotoxic effects caused by low-level occupational lead exposure. Two groups of 66 workers and 86 controls were examined with a battery including a questionnaire on neurotoxic symptoms, the measure of performance at neurobehavioral testing, the detection of visual contrast sensitivity, and the dosage of serum prolactin. Both current and cumulative exposure to lead were defined. The average PbB was 27.50 +/- 28 microg/dl (median 28, range 6-61) in the exposed and 8.11 +/- 4.47 microg/dl (median 7, range 2-21). The test results were controlled for possible confounders including age, schooling, alcohol and coffee intake. Significant differences were observed between exposed and controls regarding neurotoxic symptoms reporting, the exposed reporting more frequently mood changes and abnormal fatigue. The exposed subjects showed a decreased visual contrast sensitivity, and a marked increase of prolactin secretion. No changes emerged regarding neurobehavioral testing. The alterations observed resulted associated to the current lead exposure and not to the cumulative indices. A safe exposure level was calculated on the basis of dose-response relationship with prolactin alteration, yielding a PbB value of 10 microg/dl.
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