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BBLP
Dr. Ben Balzer Technical advisory board member The LEAD group (general practice) (Lead Education and Abatement Design Group)
6 September 2000
Lead Poisoning
Lead has no known biological function. There is no proven safe lower limit for lead. Lead Pb++, competes with Ca++, Fe++ It is cheap, useful,easy to mine, therefore Lead is ubiquitous- in air, food, water, soil, ubiquitousceilings etc. Leaded petrol means that all environmental dusts are high in lead- contaminating leadceiling dust, topsoil, window wells etc.
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Absorption of Lead
Lead goes down iron or calcium absorption pathway in GIT. Children absorb lead well orally (~50%) cf adults poorly (~10%). Children also have more hand to mouth activity. Lead absorption is enhanced if diet is poor in iron or calcium. Pica is one of the worst risk factors. Lead can be inhaled. Tetraethyl lead can be absorbed via skin.
S:\Leadgpc\BB Lead Poisoning.ppt 5
Absorption of Lead
Contribution of Sources
Distribution of Lead
95% long bones. Binds into matrix. Released during osteolysis. 4% brain,liver, kidneys. 1% blood. Crosses placenta, foetal BBB is open
Mobilization of lead from the skeleton during the post-natal period is larger than postduring pregnancy. regnancy.
Gulson BL, Mahaffey KR, Jameson CW, Mizon KJ, Korsch MJ, Cameron MA, Eisman JA. J Lab Clin Med 1998a;131:324-9 1998a;131:324-
Lead is released in menopausal bone loss Lead levels have second peak in middle ageage- more in men than women (NHANES 3). Lead follows calcium into and out of bone.
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Lead movement
In childhood, blood lead levels reflect the environmental lead level ie exogenous lead. Protection requires placing barriers between the child and the lead. In adults, lead levels reflect the release of endogenous lead from bone, as well as the intake of exogenous lead. Protection requires prevention of exposure plus 11 preservation of bone density.
Data from the US NHANES 3 study showing the second peak of lead levels in adulthood. Higher adult male levels reflect occupation and hobby. High risk occupations would be even higher. Women get a postpostmenopausal peak.
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Lead and Race. Data from the UIS NHANES 3 study showing differences with race probably reflecting differences in accommodation and occupation
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Measurable adverse behaviour changes in 2 year olds Mendelsohn 1999. Alan L. Mendelsohn, Benard P.
Dreyer, Arthur H. Fierman, Carolyn M. Rosen, Lori A. Legano, Hillary A. Kruger, Sylvia W. Lim, and Cheryl D. Courtlandt "Low-Level Lead Exposure and Behavior in Early "LowChildhood Pediatrics 1998; 101: e10
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Lead and IQ
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Toxicology of Lead 1
Lead disrupts the main structural components of the blood-brain barrier by bloodprimary injury to astrocytes with a secondary damage to the endothelial microvasculature. Within the brain, leadleadinduced damage occurs preferentially in the prefrontal cerebral cortex, hippocampus and cerebellum. Some cerebellum. characteristic clinical features of lead poisoning may be attributed to this specific anatomical pattern.
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Toxicology of Lead 3
The cellular, intracellular and molecular mechanisms of lead neurotoxicity are numerous, as lead impacts many biological activities at different levels of control: at the voltage-gated channels voltageand on the first, second and third messenger systems. These effects could systems. be related to lead's ability to interfere with the regulatory action of calcium in cell functions.
Finkelstein Y, Markowitz ME, Rosen JF Low-level leadLowleadinduced neurotoxicity in children: an update on central nervous system effects Brain Res Brain Res Rev 1998 Jul;27(2):168Jul;27(2):168-76
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Toxicology of Lead 4
At a neuronal level, exposure to lead alters the release of neurotransmitter from presynaptic nerve endings. Spontaneous release is enhanced and evoked release is inhibited. The former may be due to activation of protein kinases in the nerve endings and the latter to blockade of voltagevoltage-dependent calcium channels. This disruption of neuronal activity may, in turn, alter the developmental processes of synapse formation and result in a less efficient brain with cognitive deficits. Bressler JP, Goldstein GW
Mechanisms of lead neurotoxicity. Biochem Pharmacol 1991 Feb 15;41(4):479-84 15;41(4):479-
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Niklowitz WJ Neurofibrillary changes after acute experimental lead poisoning. Neurology 1975 Oct;25(10):927-34 Oct;25(10):927-
Following acute tetraethyllead intoxication in rabbits classic neurofibrillary tangles develop. As studied by electron microscopy, such tangles develop in hydropic degenerating neurons and consist primarily of bundles of 200 A diameter smooth tubules of enormous length. In two of 16 animals a few twisted tubules (periodicity of 800 A) also could be found. The significance of these lead-induced twisted tubules, so leadcharacteristic of Alzheimer's pre-senile predementia in man, is discussed.
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Unresolved Questions
How much does lead contribute to cognitive decline and Alzheimers disease? Do bone preserving therapies or calcium supplements reduce cognitive decline? Is lead a modifiable risk factor for dementia?
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No Yes
Have any of the following conditions sometimes associated with lead poisoning, eg iron deficiency anaemia, behaviour problem, learning problem or developmental delay?
No Yes
If your child is aged between 9 and 48 months, does he or she: y Live in, or frequently visit, a house* built before 1970 with peeling or chipping paint? y Live in, or frequently visit, a house* built before 1970 with or ongoing renovation where old paint (interior or exterior) has been burnt or sanded off, or where ceilings, walls or floors demolished? y Live in, or frequently visit, a house near a lead releasing industry, eg lead mine, lead smelter, batterybattery-recycling plant? Live with an adult whose job or hobby uses lead? (eg lead mining or smelting, automotive repair, panelpanel-beating, leadlighting, fishing sinker making, electronics, shooting instruction, car-battery carservice/ repair or manufacture).