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- Dr. Ben Balzer
- Technical Advisory Board member
- The LEAD group (general practice)
- (Lead Education and Abatement Design Group)
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- 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, ceilings etc.
- Leaded petrol means that all environmental dusts are high in lead-
contaminating ceiling dust, topsoil, window wells etc.
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- Paint (until 1970)
- Petrol (tetraethyl lead)
- Household dust (via settlement
of air pollution)
- Ceiling dust
- Occupational
- Solder
- Ceramic glazes
- Pesticides (lead arsenate)
- Cigarettes
- Mines, smelters
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- TV's, Computer monitors
- Batteries, Bullets Sinkers
- Aviation
- X-ray shields
- Crystal-ware (high levels in
decanters)
- Explosives
- Non-stick linings of pots (in
the past)
- Plastic colouring (wire, blinds)
- Pewter
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- 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.
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- 95% long bones.
- Binds into matrix.
- Released during osteolysis.
- 4% brain, liver, kidneys.
- 1% blood.
- Crosses placenta, foetal BBB is open
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- Pregnancy increases mobilization of lead from maternal skeleton
Gulson BL, Jameson CW, Mahaffey KR, Mizon KJ, Korsch MJ, Vimpani
G.. J Lab Clin Med 1997a;130:51-62
- Mobilization of lead from the skeleton during the post-natal period is
larger than during pregnancy.
Gulson BL, Mahaffey KR, Jameson CW, Mizon KJ, Korsch MJ, Cameron
MA, Eisman JA. J Lab Clin Med 1998a;131:324-9
- Lead is released in menopausal bone loss
- Lead levels have second peak in middle age- more in men than women
(NHANES 3).
- Lead follows calcium into and out of bone.
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- 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 preservation of bone density.
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- Concentration related
- IQ/ delinquency related to total dosage in childhood
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- < 0.48µmol/L (10µg/dL)
= NHMRC Goal.
- >0.48µmol/L (10µg/dL)
= elevated.
- >0.72µmol/L (15µg/dL)
=substantially elevated. Notifiable level.
- 1.20µmol/L (25µg/dL)
= dangerously elevated.
- >2.20µmol/L (45µg/dL)= Symptomatic.
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- Each 0.48 µmol/L(10µg/dL) in children.
- = 4 to 7 IQ points (US Acad.
Pediatrics).
- Industry/ Australian government consensus
of 3-5 IQ points.
- Effects on behaviour are FAR WORSE.
- Delinquency rates are 8 times higher in the top 30% of bone lead.
Needleman 1996.
Needleman, Herbert L. et al, "Bone Lead Levels and
Delinquent Behavior," JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
Vol. 275, No. 5 (February 7, 1996), pgs.363-369.
- 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
Childhood“ Pediatrics 1998; 101: e10
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- Lead disrupts the main structural components of the blood-brain barrier
by primary injury to astrocytes with a secondary damage to the
endothelial microvasculature. Within the brain, lead-induced damage
occurs preferentially in the prefrontal cerebral cortex, hippocampus
and cerebellum. Some characteristic clinical features of lead poisoning
may be attributed to this specific anatomical pattern.
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- Although the molecular targets for lead are unknown, a vast amount of
evidence accumulated over many years has shown that lead disrupts
processes that are regulated by calcium.
- Picomolar concentrations of lead can replace micromolar concentrations
of calcium in a protein kinase C enzyme assay. Furthermore, lead
activates protein kinase C in intact cells and induces the expression
of new genes by a mechanism dependent on protein kinase C. We propose
that the learning deficits caused by lead are due to events regulated
by protein kinase C that most likely occur at the synapse.
Bressler J, Kim KA,
Chakraborti T, Goldstein GMolecular mechanisms of lead neurotoxicity. Neurochem
Res 1999 Apr;24(4):595-600
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- 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 and on
the first, second and third messenger systems. These effects could 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 lead-induced neurotoxicity in children: an
update on central nervous system effects Brain Res Brain Res Rev 1998
Jul;27(2):168-76
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- 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 voltage-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
- ?Effect of lead on omega 3 and 6 fats.
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- Risk of dementia increases with lead burden
- Risk of accidental lead ingestion
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- The relationship between performance on cognitive tasks and circulating
levels of lead in blood and accumulated levels of lead in bone was
examined in 141 middle-aged and elderly men. Men with higher levels of
blood and bone (tibia) lead copied spatial figures less accurately; men
with higher levels of bone (tibia) lead had slower responses for
pattern memory. These findings suggest that low levels of lead
contribute to impairments in cognitive function among elderly men.
Payton M, Riggs KM, Spiro A 3rd, Weiss ST, Hu H Relations of
bone and blood lead to cognitive function: the VA Normative Aging
Study.
Neurotoxicol Teratol 1998 Jan-Feb;20(1):19-27
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- /~/ the cross-sectional relationship between blood lead levels and a
variety of measures of neuropsychological function in a large cohort of
elderly women /~/ This study / demonstrates that blood lead levels as
low as 8 micrograms/dl were significantly associated with poorer
cognitive function as measured by certain neuropsychological tests.
Even a slight decrement in cognition would have a large public health
impact due to the large number of elderly at risk.
- Muldoon SB, Cauley JA, Kuller LH, Morrow L, Needleman HL, Scott J,
Hooper FJ Neuroepidemiology 1996;15(2):62-72Effects of blood lead
levels on cognitive function of older women.
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- Following acute tetraethyl lead 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 characteristic of Alzheimer's pre-senile dementia in man,
is discussed.
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- How much does lead contribute to cognitive decline and Alzheimer’s
disease?
- Do bone preserving therapies or calcium supplements reduce cognitive
decline?
- Is lead a modifiable risk factor for dementia?
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- If your child is aged between 9 and 48 months, does he or she:
- Live in, or frequently visit, a house* built
before 1970 with peeling or chipping paint?
- 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?
- Live in, or frequently visit, a house near a lead releasing industry, eg lead
mine, lead smelter, battery-recycling plant?
- Live with an adult whose job or hobby uses lead? (eg lead mining or
smelting, automotive repair, panel-beating, leadlighting, fishing sinker
making, electronics, shooting instruction, car-battery service/ repair
or manufacture).
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- 1. 1978 Lead banned from paint
- 2. 1980's- Levels higher than Australia
- 3. Late 1980's Removal of lead from gasoline
- 4. 1980's Universal questionnaire screening
- 5. 1991 Universal blood testing
- 6. 1990's Public housing program
- 7. 1990's Private housing program
- 8. 1990's Massive EPA environmental program
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- 9. ~1995 Title X regulations for sale of properties
built before 1978.
- 10. ~1997 Lead litigation compensation approaches
asbestos in some states.
- 11. 1998 Builders, tradesmen required to issue
documents warning clients of risk when they renovate properties built
before 1978.
- 12. 1998 Successful reduction in community levels
leads to reintroduction of questionnaire screening in some areas.
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