High prenatal and postnatal lead exposure associated lead encephalopathy in an infant.

An 11-month-old child presented with persistent seizures requiring ventilator support. The child had global developmental delay, was staying in the premises of battery manufacturing unit, had microcytic and hypochromic anemia with basophilic stripling on peripheral smear, lead line on radiograph of the long bones and BLL of 244 µg/dl. The CT scan of the brain revealed cerebral atrophy. The mother also had high BLL and lead line in the radiograph of the long bones. The child was managed with chelation therapy. Given the continuing lead exposure among occupational and general populations in India, this case study highlights the need for prompt environmental preventive actions as well as nutritional and preventive counseling for occupational populations.

Lead encephalopathy in an infant mimicking a neurometabolic disorder.

We report the case of a 7-month-old child who presented with regression of milestones, seizures, altered sensorium, and vomiting. An elder sibling had died of similar complaints. Lead encephalopathy was considered because of presence of microcytic hypochromic anemia and dense metaphyseal bands on wrist radiogram. Magnetic resonance imaging (MRI) of the brain revealed diffuse dysmyelination involving both periventricular and subcortical white matter. Such diffuse changes have not been described previously. The child's father was operating an illicit lead-acid battery manufacturing unit at home. The child was subjected to chelation therapy, which was accompanied by environmental exposure source modification. He showed significant improvement. Our case highlights the importance of taking a detailed occupational history and considering lead poisoning in the differential diagnosis of encephalopathy of unidentifiable cause.

A coordinated relocation strategy for enhancing case management of lead poisoned children: outcomes and costs.

Controlling residential lead hazards is critical for case management of lead poisoned children. To attain this goal, permanent relocation of the family is sometimes necessary or advisable for many reasons, including poor housing conditions; extensive lead hazards; lack of abatement resources, landlord compliance and local enforcement capacity; and family eviction. During 1996-1998, the Kennedy Krieger Institute implemented a unique capitated program for case management of Baltimore City children with blood lead concentrations (PbB) >19 microg/dL. The Program provided financial, housing, and social work assistance to facilitate relocation as a means of providing safer housing. Nearly half of the Program families relocated with direct assistance, and 28% relocated on their own. The Program evaluation examined the costs and benefits of relocation. Average relocation cost per child was relatively inexpensive (<1,500 dollars). Average relocation time of 5 months (range <2 months to >12 months) was less than the 8-month average time to complete lead hazard control work in 14 city and state programs funded by U.S. HUD. Relocation was associated with (1) a statistically significant decrease in dust lead loadings on floors, windowsills and window troughs that persisted for one year, and (2) statistically significantly greater decreases in children's PbB compared to children who did not relocate from untreated homes. Children relocated to housing that met current Federal residential dust lead standards had statistically significant decreases in blood lead levels. Visual inspection did not consistently identify relocation houses with dust lead levels below current Federal standards, indicating that dust testing should be an essential component of future programs. This will require additional resources for dust testing and possibly cleaning and repairs but is expected to yield additional benefits for children. The findings support recent U.S. CDC case management recommendations suggesting that permanent relocation to safer housing is a viable means to reduce children's lead exposure. The benefits of relocation notwithstanding, 40% of families moved at least twice. Research is needed to better understand how to expedite relocation and encourage families to remain in safe housing. Relocation does not negate owners' and health authorities' responsibilities to address lead hazards in the child's original house in order to protect future occupants.

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.

Enriched environment during development is protective against lead-induced neurotoxicity.

It is known that children of lower socioeconomic status have a disproportionately higher risk of being exposed to lead and have a more negative outcome from that exposure than children who are raised under more fortunate circumstances. Yet, little is known about how environmental factors may influence the injurious effects on the brain of a neurotoxin such as lead. The present study used an animal model of lead poisoning to examine the extent to which different environmental milieus may modify the effects of lead on the developing brain. Young rats were raised in either enriched or impoverished environments and drank either distilled water or water with lead. Lead-exposed rats raised in the impoverished environment had spatial learning deficits and significantly decreased neurotrophic factor gene expression in the hippocampus. In contrast, the animals raised in the enriched environment were significantly protected against the behavioral and neurochemical toxicity of lead. These results demonstrate that impoverished environment may accentuate while enriched environment may ameliorate neurobehavioral and neurochemical toxicity from developmental lead exposure.

Pseudotumor cerebral maligno en niños por intoxicación plumbica / Lead poisoning presenting as malignant pseudotumor cerebri in children

Introducción: El pseudotumor cerebral (PTC), o hipertensión endocraneana benigna, se caracteriza por sintomatología compatible con aumento de la presión endocraneana en ausencia de lesión espacio-ocupante o dilatación ventricular por obstrucción en la circulación del LCR. Se presenta con cefalea, náuseas-vómitos, y variadas alteraciones visuales con edema de papila. Las causas subyacentes son múltiples: alteraciones endocrinas y metabólicas, obesidad, medicamentos, trombosis senos venosos, megadosis de vitamina A, sinusopatías, etc. como así también intoxicación plúmbica. Objetivo: Detectar etiología tóxica en pacientes con PTC en los cuales no se evidenció factor causal mediante interrogatorio dirigido a pesquisa de fuentes contaminantes de plomo. Material y Métodos: Análisis prospectivo de pacientes ambulatorios o internados con diagnóstico de PTC. Estudios de Rx de cráneo, oftalmológicos y neuroimágenes. Aplicación de protocolo de investigación de contacto con plomo. Determinaciones en sangre y orina del bioperfil plúmbico: ALA-D, ALA-U, plombemia, PPE, coproporfirinas III. Comparación con grupo control de los niños intoxicados. Aplicación del test de Fisher. Resultados: Fueron evaluados 66 niños entre 4 meses y 13 años, 49 varones. Las manifestaciones clínicas fueron: cefalea (85 por ciento), náuseas-vómitos (94 por ciento), alteraciones visuales: diplopia, disminución agudeza visual, estrabismo (91 por ciento), edema de papila (89 por ciento). Hipertensión radiológica (55 por ciento). Neuroimágenes: negativas para tumor (100 por ciento), compatible con edema cerebral (27 por ciento). Los factores etiológicos fueron identificados en 55 casos (83 por ciento) obesidad, endocrinopatía, corticoterapia, megadosis de vitamina A, sinusopatías, etc. En el 17 por ciento restante (11 casos) se sospechó etiología tóxica, comprobándose intoxicación plúmbica en 8 niños (12 por ciento). Conclusiones: Sugerimos aplicar interrogatorio dirigido hacia pesquisa de fuentes contaminantes de plomo en casos de PTC sin causa establecida, y confirmación con análisis de nivel de plomo en sangre y bioperfil plúmbico. El diagnóstico y tratamiento oportunos evitarán el pronóstico desfavorable de la afección, por eso consideramos como "maligno" a este tipo de pseudotumor. (AU)