Lead in a case of encephalopathy.

A 2-year-old boy with a history of pica was admitted with vomiting and treated overnight for viral tonsillitis. A week later, he presented with a prolonged afebrile seizure and required intubation and ventilation. Antibiotics and acyclovir were started. Despite extensive investigations including MRI head, no cause was identified. Four days later, he deteriorated with signs of raised intracranial pressure. On day 5, blood lead concentration in the sample collected at admission was reported as grossly elevated, consistent with a diagnosis of severe lead poisoning from ingesting lead-containing paint at the family home. Chelation therapy was started but, unfortunately, he did not make a neurological recovery, and care was withdrawn. A serious case review identified a lack of awareness of lead poisoning and its relation to pica as a root cause. We report this case to share our experience and the importance of considering lead poisoning in children with pica.

Role of chelation in the treatment of lead poisoning: discussion of the Treatment of Lead-Exposed Children Trial (TLC).

Lead exposure in children is one component leading to cognitive impairment. The Treatment of Lead-Exposed Children Trial (1994-2004) studied the effect of succimer in treating low levels of lead exposure (20-44 mcg/dL) in children 12 to 33 months old. While succimer was effective in reducing blood lead concentrations in the short term, treatment of blood lead levels did not result in any detectable improvement in a wide variety of measurements of cognitive or behavioral function. Furthermore, blood lead concentrations were not distinguishable between chelated and non-chelated individuals at 1 year. The most important treatment strategy is identification and termination of major sources of lead exposure.

Lead poisoning among Burmese refugee children--Indiana, 2009.

Recent routine screening revealed multiple cases of unexplained lead poisoning among children of Burmese refugees living in Fort Wayne, Indiana. A cross-sectional study was conducted to determine (a) the prevalence of elevated blood lead levels (BLLs) among Burmese children and (b) potential sources of lead exposure. A case was defined as an elevated venous BLL (≥10 µg/dL); prevalence was compared with all Indiana children screened during 2008. Environmental and product samples were tested for lead. In all, 14 of 197 (7.1%) children had elevated BLLs (prevalence ratio: 10.7) that ranged from 10.2 to 29.0 µg/dL. Six cases were newly identified; 4 were among US-born children. Laboratory testing identified a traditional ethnic digestive remedy, Daw Tway, containing a median 520 ppm lead. A multilevel linear regression model identified daily use of thanakha, an ethnic cosmetic, and Daw Tway use were related to elevated BLLs (P < .05). Routine monitoring of BLLs among this population should remain a priority.

The relation of lead neurotoxicity to the event-related potential P3b component in Inuit children from arctic Québec.

The event-related potential (ERP) P3b, a cognitive electrophysiological measure that has been linked to working memory processing in many experimental paradigms, was measured in Inuit children from Nunavik (Arctic Québec, Canada) to assess lead (Pb) neurotoxicity. Visual and auditory oddball paradigms were administered at 5 (N=27) and 11 (N=110) years of age, respectively, to elicit this ERP component. Pearson correlations and multiple regression analyses were performed to examine the associations between Pb levels and P3b parameters (peak latency and amplitude). Greater prenatal Pb exposure was related to a decrease in P3b amplitude at 5 years of age, and early childhood Pb exposure was associated with delayed P3b latency at 5 years. No significant association was observed at 11 years. These results, in line with those from previous neurobehavioral studies, suggest that Pb exposure affects cognitive processing in children even though the Pb levels measured in a large majority of our sample were below the threshold value for public health intervention used by federal agencies. This study strengthens the arguments for reducing sources of Pb exposure in Nunavik and for lowering the blood Pb concentrations considered "acceptable" in governmental policies.

Neurophysiologic and neurocognitive case profiles of Andean patients with chronic environmental lead poisoning.

This report presents case profiles of three siblings in a family of lead (Pb) glazing workers living in a Pb-contaminated Andean village who presented with extreme plumbism (blood Pb levels: 47 to 128 microg/dl) from childhood to adolescence. These cases are examples of persons who have chronic Pb poisoning as a result of prolonged occupational and environmental exposure in a Pb-glazing ceramic cottage industry in the study area. Using behavioral and physiological techniques for measuring the integrity of the peripheral and central auditory systems, including otoacoustic emissions, and replicated auditory brainstem electrophysiological potentials, the authors found normal auditory neurosensory function in each patient, thus ruling out hearing impairment as a basis for adverse neurocognitive outcomes. This finding is contrary to the prevailing view regarding the detrimental effects of Pb poisoning on the cochlear and auditory brainstem of children. Performance on tests of visual spatial intelligence and auditory memory/attention was below average in these patients, which may underlie their reported learning disabilities. In two of the cases, there was an improvement in cognitive performance following a lowering of PbB levels from chelation therapy and Pb prevention education, suggesting some level of reversibility of their neurocognitive deficits. Nevertheless, these case profiles suggest that if the patients persist in Pb-glazing activities, in spite of repeated chelation therapy and family counseling, they may continue to be re-intoxicated and remain at risk for learning disabilities and other neurological impairments.

Very low lead exposures and children's neurodevelopment.

PURPOSE OF REVIEW: We remain far from achieving the goal of eliminating lead-associated neurodevelopmental morbidities in children. New evidence regarding the blood lead levels at which morbidities occur have led to calls for the Centers for Disease Control and Prevention to reduce the current screening guideline of 10 microg/dl. The review evaluates the basis for these calls. RECENT FINDINGS: Adverse outcomes, such as reduced intelligence quotient and academic deficits, occur at levels below 10 microg/dl. Some studies suggest that the rate of decline in performance is greater at levels below 10 microg/dl than above 10 microg/dl, although a plausible mechanism has not been identified. Increased exposure is also associated with neuropsychiatric disorders such as attention deficit hyperactivity disorder and antisocial behavior. Functional imaging studies are beginning to provide insight into the neural substrate of lead's neurodevelopmental effects. Current protocols for chelation therapy appear ineffective in preventing such effects, although environmental enrichment might do so. SUMMARY: No level of lead exposure appears to be 'safe' and even the current 'low' levels of exposure in children are associated with neurodevelopmental deficits. Primary prevention of exposure provides the best hope of mitigating the impact of this preventable disease.

Effects of chronic lead exposure on 1H MRS of hippocampus and frontal lobes in children.

The authors performed IQ testing and magnetic resonance spectroscopy on six lead-exposed and six control children. Levels of N-acetyl aspartate (neuronal density and mitochondrial metabolism), creatine + phosphocreatine (phosphate metabolism), and choline (membrane turnover) were decreased in four brain regions (left and right frontal, left and right hippocampus) in lead-exposed children vs controls. The reductions were right frontal > left frontal > hippocampus but were the same bilaterally in the hippocampus.

Elevated blood lead levels among children living in a fishing community, Karachi, Pakistan.

Lead is a widespread environmental contaminant worldwide and is associated with adverse outcomes in children, including impaired neurobehavioral development and learning difficulties. A cross-sectional survey of 53 young children was conducted in a fishing village on an island adjacent to Karachi, Pakistan. Whole blood from each individual was tested for lead levels. Also tested were samples of cooked food, house dust, and drinking water from 36 households. Laboratory determinations were made by the Pakistan Council for Scientific and Industrial Research with quality control by the United States Centers for Disease Control and Prevention. Fifty-two subjects (98%) had blood lead levels above 10 microg/dl (mean 21.60 microg/dl), an internationally recognized threshold for potential neurotoxicity. The mean concentration was 3.90 microg/g in cooked food, 4.02 microg/l in drinking water, and 91.30 microg/g in house dust. These findings indicate possible major health concerns and suggest significant environmental contamination in this community as well as the need to identify locally relevant early childhood exposures.