Lead Paint: Blood Brain Barrier

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Lead encephalopathy treated by versenate (CA-EDTA).

Eur Neurol. 1982;21(3):157-60.

Abstract

A patient with generalised epileptic seizures, mental and psychotic signs was diagnosed as suffering from lead encephalopathy. He was a big consumer of home-made arrack, illicit alcohol prepared at home in secrecy, in tools containing copper and lead. Basophilic stippling increased the possibility of lead encephalopathy, which was soon proved. He was successfully treated with low doses of Versenate, a chelating factor, and totally recovered.

 

Postgrad Med J. 1991 Jan;67(783):63-5.

An oral treatment for lead toxicity.

Source

Northwick Park Hospital, Harrow, Middlesex, UK.

Abstract

Chronic lead poisoning has traditionally been treated by parenteral agents. We present a case where a comparison of ethylene diaminetetra-acetic acid was made with 2,3-dimethyl succinic acid (DMSA) which has the advantage of oral administration associated with little toxicity and appeared to be at least as efficacious.

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Chronic lead poisoning: induced psychosis in an adult?

Am J Forensic Med Pathol. 2002 Mar;23(1):101.

PMID:
11953505
[PubMed – indexed for MEDLINE]
Neurology. 1978 May;28(5):507-10.

Acute and chronic progressive encephalopathy due to gasoline sniffing.

Abstract

Acute encephalopathy caused by gasoline sniffing is well recognized, but has been thought to be completely reversible. We report a patient who developed a progressive encephalopathy characterized by ataxia, tremor and dementia following repeated, deliberate gasoline inhalation. Blood and urine lead levels were consistently elevated and at autopsy, the formalin-fixed brain lead content was between 5200 and 6500 micrograms/100 gm of tissue. This case shows that repeated gasoline sniffing can result in irreversible encephalopathy and that both the acute and chronic encephalopathy probably result from organic lead intoxication and not from the gasoline itself.

 

Can Med Assoc J. 1982 Dec 15;127(12):1195-7.

Gasoline sniffing and lead encephalopathy.

Abstract

Gasoline sniffing is endemic in northern Manitoba and perhaps throughout much of northern Canada. Its most serious complication is lead encephalopathy, which can be fatal. Most of the toxic effects are thought to be due to tetraethyl lead and its metabolites. The specific treatment is chelation therapy, for which a protocol has been developed at the Health Sciences Centre, Winnipeg. Lead encephalopathy, however, is a manifestation of social, cultural and psychologic malaise.

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[Implication of lead poisoning in psychopathology of Vincent van Gogh].

imagesCACKQIAM

[Article in Spanish]

Abstract

The authors, by means of documental research, study the possibility that the physical and psychic symptoms of Vincent van Gogh may have been due to chronic lead poisoning. The technique and materials used by Van Gogh are analysed as the cause of repeated exposure to lead as well as the possible means of penetration of the metal. Through historical-biographical analysis, the progressive symptoms of the illness are compared with those of lead poisoning. The authors conclude that the excessive and continuous use by Van Gogh of pigments which were highly toxic due to their high lead content, such as white lead (lead carbonate) and yellow chrome (lead chromium), could have penetrated his organism by digestive system (primarily) in minimal daily amounts, giving rise to a clinical condition of chronic lead poisoning. This type of poisoning coincides with the clinical symptoms Van Gogh describes in his autographed letters: initial debilitation, stomatitis with loss of teeth, recurring abdominal pains, anaemia (with a “plumbic” skin tone), neuropathy of the radial and saturnine encephalopathy including epileptic crises, progressive character changes and periods of delirium. The clinical symptoms shown by Van Gogh meet present criteria for diagnosis of Organic Mental Disorder due to cerebral lesion or somatic illness (F.06; CIE-10) (DSM-IV-R), and Organic Character Disorder (F.07; CIE-10) (DSM-IV-R).

[Goya, Fortuny, Van Gogh, Portinari: lead poisoning in painters across three centuries].

[Article in Spanish]

Source

Servicio de Medicina Interna, Hospital Meixoeiro, Vigo. julio.montes.santiago@sergas.es

Abstract

Patobiographic data of four brilliant painters who lived in three different centuries (Goya [XVIII], Fortuny and Van Gogh [XIX] and Portinari [XX]), were examined in search for a suspected lead poisoning. It is concluded that Goya’s disease and deafness was probably caused by lead poisoning. Fortuny’s death was probably precipitated by this illness in conjunction with malaria. This diagnosis is more problematic in Van Gogh and only a monograph favouring this was found. Portinari certainly suffered from lead poisoning and that finally caused his death. This source of the possible poisoning could be the high lead content of their paintings.

PMID:
16604740
[PubMed – indexed for MEDLINE]

 

Is lead exposure in early life an environmental risk factor for Schizophrenia? Neurobiological connections and testable hypotheses.

Neurotoxicology. 2012 Jun;33(3):560-74. Epub  2011 Dec 9.

Source

Department of Environmental Health Sciences, Columbia University Mailman School of Public Health, New York, NY 10032, United States. trguilarte@columbia.edu

Abstract

Schizophrenia is a devastating neuropsychiatric disorder of unknown etiology. There is general agreement in the scientific community that schizophrenia is a disorder of neurodevelopmental origin in which both genes and environmental factors come together to produce a schizophrenia phenotype later in life. The challenging questions have been which genes and what environmental factors? Although there is evidence that different chromosome loci and several genes impart susceptibility for schizophrenia; and epidemiological studies point to broad aspects of the environment, only recently there has been an interest in studying gene × environment interactions. Recent evidence of a potential association between prenatal lead (Pb(2+)) exposure and schizophrenia precipitated the search for plausible neurobiological connections. The most promising connection is that in schizophrenia and in developmental Pb(2+) exposure there is strong evidence for hypoactivity of the N-methyl-d-aspartate (NMDA) subtype of excitatory amino acid receptors as an underlying neurobiological mechanism in both conditions. A hypofunction of the NMDA receptor (NMDAR) complex during critical periods of development may alter neurobiological processes that are essential for brain growth and wiring, synaptic plasticity and cognitive and behavioral outcomes associated with schizophrenia. We also describe on-going proof of concept gene-environment interaction studies of early life Pb(2+) exposure in mice expressing the human mutant form of the disrupted in schizophrenia 1 (DISC-1) gene, a gene that is strongly associated with schizophrenia and allied mental disorders.

Copyright © 2011 Elsevier Inc. All rights reserved.

Organic lead encephalopathy: behavioral change and movement disorder following gasoline inhalation.

J Clin Psychiatry. 1982 Feb;43(2):70-2.

Abstract

A 15 year old boy was evaluated in the psychiatric emergency room for the acute onset of “confusion,”insomnia, headache, and shaking of one week’s duration. Two days later hallucinations, formication and a movement disorder emerged characterized by action tremor, myoclonus, chorea and ataxia. Further history revealed inhalation of gasoline for its euphoric effects. Plasma lead levels were in the toxic range. Chelation therapy reversed the clinical symptoms. Behavioral changes and a movement disorder in the context of gasoline inhalation are highly suggestive of organic lead encephalopathy. Recognition of this syndrome is important as chelation therapy is effective.

PMID:
7056707
[PubMed – indexed for MEDLINE]

Blood Lead Level in Children with Encephalopathy

Javed H Hussain

Children’s Hospital, Boston; Harvard Medical School, 300, Longwood Ave, Boston, MA 02215, USA. javed.hussain@childrens.harvard.edu

No other heavy metal toxicity has gained as much public attention as lead – due to its impact on the developing brain of young children. Lead is ubiquitous in our environment but has no physiologic role in our biological systems. Lead became part of our daily life due to its easy workability, low melting point and corrosion-resistance. Later in our industrial society, it became part of house paint due its shining and lasting function and also used in gasoline for its anti-knock properties.

The toxicity of lead comes from its ability to mimic other biologically important metals, most notably calcium, iron and zinc, which act as cofactors in many enzymatic reactions. Lead is able to bind to enzymes delta-aminolevulinic acid dehydratase, and ferrochelatase, affecting the biosynthesis of heme causing anemia.

Lead also interferes with excitatory neuro-transmission by glutamate, which is the transmitter at more than half the synapses in the brain and is critical for learning. N-methyl-D-aspartate (NMDA) receptor, thought to be associated with neuronal development and plasticity, is blocked selectively by lead. This disrupts long-term potentiation, which compromises the permanent retention of newly learned information(1). Lead exposure also decreases the amount of NMDA receptor gene and protein in hippocampus(2).

Continue reading “Blood Lead Level in Children with Encephalopathy”

Lead encephalopathy treated by versenate (CA-EDTA).

Eur Neurol. 1982;21(3):157-60.

Abstract

A patient with generalised epileptic seizures, mental and psychotic signs was diagnosed as suffering from lead encephalopathy. He was a big consumer of home-made arrack, illicit alcohol prepared at home in secrecy, in tools containing copper and lead. Basophilic stippling increased the possibility of lead encephalopathy, which was soon proved. He was successfully treated with low doses of Versenate, a chelating factor, and totally recovered.

PMID:
6811276
[PubMed – indexed for MEDLINE]

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