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Lead Poisoning

 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.

Uses and Sources of Lead 
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


Computer monitors Batteries. Bullets Sinkers Aviation X-ray shields CrystalCrystal-ware (high levels in decanters) Explosives NonNon-stick linings of pots (in the past) Plastic colouring (wire. blinds) Pewter 4 .More Uses and Sources of Lead          TV's.

ppt 5 .  Lead absorption is enhanced if diet is poor in iron or calcium.  Lead can be inhaled. Children also have more hand to mouth activity.Absorption of Lead  Lead goes down iron or calcium absorption pathway in GIT.  Tetraethyl lead can be absorbed via skin.  Children absorb lead well orally (~50%) cf adults poorly (~10%).  Pica is one of the worst risk factors. S:\Leadgpc\BB Lead Poisoning.

Absorption of Lead 6 .

Contribution of Sources 7 .

Reduction of Lead hazards in the home  8 .

liver. foetal BBB is open 9 . kidneys.  4% brain.Distribution of Lead  95% long bones.  1% blood.  Binds into matrix.  Released during osteolysis.  Crosses placenta.

 Lead follows calcium into and out of bone. Eisman JA. regnancy.Release of lead during osteolysis  Pregnancy increases mobilization of lead from maternal skeleton Gulson BL. Korsch MJ. Cameron MA. Jameson CW. J Lab Clin Med 1997a. Jameson CW. Mahaffey KR.130:51-62 1997a.more in men than women (NHANES 3).130:51-  Mobilization of lead from the skeleton during the post-natal period is larger than postduring pregnancy.. Gulson BL. 10 . Mizon KJ. Korsch MJ. Mahaffey KR. Vimpani G.131:324-9 1998a. J Lab Clin Med 1998a.131:324-  Lead is released in menopausal bone loss  Lead levels have second peak in middle ageage. Mizon KJ.

as well as the intake of exogenous lead.  In adults. .Lead movement  In childhood. Protection requires prevention of exposure plus 11 preservation of bone density. blood lead levels reflect the environmental lead level ie exogenous lead. lead levels reflect the release of endogenous lead from bone. Protection requires placing barriers between the child and the lead.

12 . Women get a postpostmenopausal peak.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.

Lead and Race. Data from the UIS NHANES 3 study showing differences with race ²probably reflecting differences in accommodation and occupation 13 .

Health Effects of Lead  Concentration related  IQ/ delinquency related to total dosage in childhood 14 .

 >0.15 . Notifiable level.72µmol/l (15µg/dl) =substantially elevated.Recommended Lead level <0.  >2.20µmol/l (45µg/dl)= Symptomatic.20µmol/l (25µg/dl) = dangerously elevated.48µmol/l (10µg/dl) = NHMRC Goal.  >0.48 (10µg/dl)  < 0.48µmol/l (10µg/dl) = elevated.  1.

Symptoms from lead are rare! 16 .

275. Courtlandt "Low-Level Lead Exposure and Behavior in Early "LowChildhood´ Pediatrics 1998. 3 Effects on behaviour are FAR WORSE.  Industry/ Australian government consensus of 3-5 IQ points. Dreyer. Carolyn M. Rosen. Hillary A. and Cheryl D. Benard P. Legano. Alan L. 5 (February 7. 1996). Kruger.363369. Mendelsohn. et al. Arthur H. Sylvia W. "Bone Lead Levels and Delinquent Behavior.  Delinquency rates are 8 times higher in the top 30% of bone lead. Herbert L. = 4 to 7 IQ points (US Acad. Pediatrics). Lori A. Needleman 1996. 101: e10 17 . pgs." JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION Vol.363pgs.Lead and Neurodevelopment  Each 0. Needleman.48 µmol/l(10µg/dl) in children. Fierman.  Measurable adverse behaviour changes in 2 year olds Mendelsohn 1999. No. Lim.

Lead and IQ 18 .

Within the brain. hippocampus and cerebellum. Some cerebellum.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. characteristic clinical features of lead poisoning may be attributed to this specific anatomical pattern. 19 . leadleadinduced damage occurs preferentially in the prefrontal cerebral cortex.

a vast amount of evidence accumulated over many years has shown that lead disrupts processes that are regulated by calcium. 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.24(4):59520 . Bressler J. Goldstein GMolecular mechanisms of lead neurotoxicity. lead activates protein kinase C in intact cells and induces the expression of new genes by a mechanism dependent on protein kinase C.24(4):595-600 Apr.Toxicology of Lead contd Although the molecular targets for lead are unknown.  Picomolar concentrations of lead can replace micromolar concentrations of calcium in a protein kinase C enzyme assay. Kim KA. Furthermore. Chakraborti T. Neurochem Res 1999 Apr.

These effects could systems. Finkelstein Y.27(2):168Jul.27(2):168-76 21 . Markowitz ME. second and third messenger systems. Rosen JF Low-level leadLowleadinduced neurotoxicity in children: an update on central nervous system effects Brain Res Brain Res Rev 1998 Jul. be related to lead's ability to interfere with the regulatory action of calcium in cell functions.Toxicology of Lead 3 The cellular. as lead impacts many biological activities at different levels of control: at the voltage-gated channels voltageand on the first. intracellular and molecular mechanisms of lead neurotoxicity are numerous.

alter the developmental processes of synapse formation and result in a less efficient brain with cognitive deficits. Biochem Pharmacol 1991 Feb 15. Bressler JP. exposure to lead alters the release of neurotransmitter from presynaptic nerve endings. Goldstein GW Mechanisms of lead neurotoxicity. This disruption of neuronal activity may.41(4):479-84 15. The former may be due to activation of protein kinases in the nerve endings and the latter to blockade of voltagevoltage-dependent calcium channels. Spontaneous release is enhanced and evoked release is inhibited.Toxicology of Lead 4  At a neuronal level.41(4):479-  ?Effect of lead on omega 3 and 6 fats. in turn. 22 .

Lead and the Elderly  Risk of dementia increases with lead burden  Risk of accidental lead ingestion 23 .

These findings suggest that low levels of lead contribute to impairments in cognitive function among elderly men.20(1):19- . Neurotoxicol Teratol 1998 Jan-Feb. Weiss ST. Hu H Relations of bone and 24 blood lead to cognitive function: the VA Normative Aging Study. Spiro A 3rd.Dementia and lead 1  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 middlemiddle-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.20(1):19-27 Jan-Feb. Payton M. Riggs KM.

Even a slight decrement in cognition would have a large public health impact due to the large number of elderly at risk. Kuller LH.15(2):62-72Effects of blood lead 1996. Needleman HL. Scott J. Morrow L.15(2):62-72Effects levels on cognitive function of older women.Dementia and Lead 2  /~/ the cross-sectional relationship crossbetween 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. . 25 Hooper FJ Neuroepidemiology 1996. Cauley JA.  Muldoon SB.

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. is discussed. 26 . In two of 16 animals a few twisted tubules (periodicity of 800 A) also could be found.25(10):927-34 Oct. Neurology 1975 Oct. so leadcharacteristic of Alzheimer's pre-senile predementia in man.Niklowitz WJ Neurofibrillary changes after acute experimental lead poisoning. The significance of these lead-induced twisted tubules.

Unresolved Questions  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? 27 .

28 .Incidence of Elevated Blood Leads Sydney 1996 Mira Et Al.

Childhood Risk Factor Questionnaire Does your child«. Have a brother or sister. behaviour problem. learning problem or developmental delay? No Yes . eg iron deficiency anaemia. housemate or playmate with an elevated blood lead level? No Yes Sometimes eat non-food items such as soil or paint? No Yes Have any of the following conditions sometimes associated with lead poisoning.

a house* built before 1970 with peeling or chipping paint? y Live in. a house* built before 1970 with or ongoing renovation where old paint (interior or exterior) has been burnt or sanded off. batterybattery-recycling plant? Live with an adult whose job or hobby uses lead? (eg lead mining or smelting. lead smelter. eg lead mine. or frequently visit. walls or floors demolished? y Live in. or frequently visit. . a house near a lead releasing industry. electronics. shooting instruction.If your child is aged between 9 and 48 months. car-battery carservice/ repair or manufacture). automotive repair. panelpanel-beating. does he or she: y Live in. or where ceilings. fishing sinker making. leadlighting. or frequently visit.

Lead Situation 1  1. 1980's.Levels higher than Australia 1980's 3.U. 1990's Massive EPA environmental program 31 . 1990's Private housing program  8. 1978 Lead banned from paint  2.S. 1980's Universal questionnaire screening  5. 1990's Public housing program  7. Late 1980's Removal of lead from gasoline  4. 1991 Universal blood testing  6.

1998 Builders. tradesmen required to issue documents warning clients of risk when they renovate properties built before 1978.S. Lead Situation 2  9.  11.U.  10. 32 .  12. 1998 Successful reduction in community levels leads to reintroduction of questionnaire screening in some areas. ~1995 Title X regulations for sale of properties built before 1978. ~1997 Lead litigation compensation approaches asbestos in some states.