Lead is the most common metal involved in chronic poisoning. It has been widely used for over 2000 years in domestic, industrial, and medical applications. Lead toxicity affects virtually all organs and systems of the body. Symptoms of chronic lead poisoning range from mild effects like fatigue and abdominal pain to more severe effects like lead encephalopathy. Treatment involves chelating agents like calcium disodium EDTA that help remove lead from the body.

2.  Leadisthecommon
estmetalinvolvedinchronicpoisoning.
Itwasoneofthefirstmetalsknowntom
a
n
andhasbeenwidelyusedduringthelasttwo
thousandyearsfordomestic,industrial,andtherapeuticpurposes.
 Leadisabundantinsoil,beingdistributedthroughouttheearth’scrust.

3.  ThemainuseofPbisintheproductionofstoragebatteriesandinsheathing
electriccables.
 Itisalsousefulasprotectiveshieldingfromx-raysandradiationfromnuclearreactors.
 Certainfolkmedicines(eg,theMexicanremediesandsomeIndianAyurvedic
preparations)maycontainhighamountsofleadsalts.

4.  Leadacetate(sugaroflead)hasbeenusedintherapeutics,
 leadcarbonate(whitelead)isstillusedinpaints,
 lead oxide (litharge) is essential for glazing of pottery and enamel ware, and
Tetraethylleadismixedwithpetrolasanantiknocktopreventdetonationininternal
combustionengines.
 A
m
on
g cosm
etics,leadtetro
xide is th
e m
ost com
m
oncom
poun
din“Sin
door”
an
dleadsulfidein“Surma”

5.  Candlewithlead-containingwicks
 Ayurvedicmedicines
 Paint
 Retainedbullets
 Ink
 Automobile storage battery casing;battery repairshops
 Ceramicglazes
 Leadpipes
 Silverjewelleryworkers
 Renovation/modernisationofoldhomes.

6.  Pbtoxicityaffects virtuallyallorgansandsystemsofthebody
 TheproposedmechanismofPbtoxicityinvolvesitsabilitytoinhibitormimictheactionofcations
suchascalcium,zinc,andiron,andtointerferewithvitalproteinsbybindingtosulfhydryl,amine,
phosphate,andcarboxylgroups.
 PbincreasesintracellularlevelsofCalciuminbraincapillaries,neurons,hepatocytes,andarteriesthat
triggersmoothmusclecontraction,therebyinducinghypertension

7.  Pbinterfereswithhemebiosynthesisbyinterferingwithferrochelatase,A
L
A
S
(aminolevulinicacidsynthetase),andA
L
A
D(aminolevulinicaciddehydrase).Therefore,
decreasedhemoglobinandanemiaresultsinindividualsexposedtoexcessivePb
 Leadincreaseshaemolysisasaresultofwhichimmatureredcellsarereleasedintocirculation
suchasreticulocytesandbasophilic stippledcells (theresultofaggregationof
ribonucleicacidduetoinhibitionoftheenzymepyrimidine-5-nucleotidasewhichnormally
eliminatesdegradedR
N
A
)

8.  Inthenervoussystem,PbsubstitutesforCaasasecondarymessengerinneurons,blocking
voltage-gatedCachannels,inhibitinginfluxofCaandsubsequentreleaseof
neurotransmitter.Theresultisaninhibitionofsynaptictransmission.
 Pbinhibitsglutamateuptakeandglutamatesynthetaseactivityinastroglia,thus
inhibitingtheregenerationofglutamate,amajorexcitatoryneurotransmitter
 Thisleadstodecreasednerveconduction,increasedpsychomotoractivity,lowerIQ,
andbehavioural/learningdisorders.

9.  Leadalsohasdeleteriouseffectso
ntheC
V
S(hypertensionandmyocarditis),kidney
(nephritis),andreproductiveorgans(infertility).
 Inaddition,leadcandecreaseuricacidrenalexcretion,therebyraisingblooduratelevels
andpredisposingtogout

10. Thisisnotreallyrelevanttoleadsinceacute
poisoningisveryrare.
Theaveragelethaldoseissaidtobe10gm/70kgformostleadsalts,whileitis100mg/kgfor
tetraethyllead.
 Todaytheacceptedupperlevelforbloodlead(BL)isfixedas35mcg/100ml.
 Howevertherearereportsthatadverseeffectsespeciallyo
nthehaematopoieticsystemcan
occuratlevelsaslowas10mcg/100ml.

11.  NeurobehaviouraldisordersinchildrencanoccuratB
L
aslowas25mcg/100ml.
 Hence,thecurrentlyevenlevelsaslowas10mcg/100m
lasunacceptable,
especiallyinchildren.

12. Absorption
Leadisabsorbedthroughallportalsofentry
 Occupationalexposureresultsmainlyfrominhalation,whileinmostothersituationsthem
o
d
eof
intakeisingestion.
 Tetraethylleadcanbeabsorbedrapidlythroughintactskin.
 About 5–15 of ingested lead is absorbed byadults with less than 5 retained.
 Children,however,absorbapproximately 5
0 of ingested lead and retainabout 3
0 .

13. Distribution
 lead is distributed amon
gthreecompartments:blood, softtissuesandthemineralizing
tissues(bonesandteeth).
 Leadis distributed to those areas of the skeleton which are growing mostrapidly.
 These include the radius,tibia, andfemur,which are the mostmetabolicallyactive
 itisstoredinthebonesasphosphateandcarbonate.

14.  Inchildrenabout70
tissues.
oftotalbodyleadisskeletal,whileinadultsover95
isin
osseous
 Significantamountsofskeletalleadarereleasedfromboneintothebloodstreamperiodicallyresulting
insymptomsoftoxicity.
 Theconditionsfavouringthisincludeacidosis,fevers,alcoholicintake,andevenexposureto
sunlight.
Elimination
 Excreted primarily in the urine (about 65 ) andbile (about 35 ).

15. Acute poisoning
 Thisisrare.Man
yreportedcasesofacutepoisoningmayactuallybeexacerbationsofchronic
leadpoisoningwhensignificantquantitiesofleadaresuddenlyreleasedintothebloodstream
frombone.
 Symptomsincludemetallictaste,abdominalpain,constipationordiarrhoea(stoolsmaybe
blackishduetoleadsulfide),vomiting,hyperactivityorlethargy,ataxia,behaviouralchanges,
convulsions,andcoma.

16. Chronic Poisoning
 Subacuteorchronicexposureismorec
o
m
m
o
n
thanacutepoisoning
 Constitutionaleffectsincludefatigue,malaise,irritability,anorexia,insomnia,weightloss,decreased
libido,arthralgias,andmyalgias.
 Hypertensionmaybeassociatedwithleadexposureinsusceptiblepopulations
 Gastrointestinaleffectsincludecrampyabdominalpain(leadcolic),nausea,constipation,or(less
commonly)diarrhea.

17.  Centralnervoussystemmanifestationsrangefromimpairedconcentration,headache,diminishedvisual-
motorcoordination,andtremortoovertencephalopathy(alife-threateningemergencycharacterizedby
agitateddeliriumorlethargy,ataxia,convulsions,andcoma).
 Chroniclow-levelexposureininfantsandchildrenmayleadtodecreasedintelligenceandimpaired
neurobehavioraldevelopment,stuntedgrowth,anddiminishedauditoryacuity
 Peripheralmotorneuropathy,affecting mainlytheupperextremities,cancausesevereextensormuscle
weakness(“wristdrop”)

18.  Hematologiceffectsincludenormochromicormicrocyticanemia,whichmaybe
accompaniedbybasophilicstippling.Hemolysismayoccur.
 Nephrotoxiceffectsincludereversibleacutetubulardysfunctionandchronic
interstitialfibrosis.Hyperuricemiaandgoutmayoccur.
 Adversereproductiveoutcomesmayincludediminishedoraberrantspermproduction,
increasedrateofmiscarriage,pretermdelivery,decreasedgestationalage,lowbirth
weight,andimpairedneurologicdevelopment.

19. MildToxicity(BL4
0to6
0
mcg/100ml):
ModerateToxicity(BL6
0to
100mcg/100ml):
SevereToxicity(BLmorethan100
mcg/100ml):
Myalgia
Paraesth
esia
Fatigue
Irritability
Abdominaldiscomfort
–Arthralgia(especially
nocturnal)
– Muscularexhaustibility
–Tremor
– Headache
– Diffuseabdominalpain
–Anorexia,metallictaste,
vomiting
– Constipation
–Weightloss
– Hypertension.
–Leadpalsy:wristdrop)orfootdrop.
–Abluishblackleadlineongums
(Burton’sline)
–Leadcolic:intermittentsevere
abdominalcramps.
–Leadencephalopathy:Itismore
c
o
m
m
o
n
inchildrenandisoften
associatedwithorganicleadtoxicity,
especiallytetraethylleadorTEL.

21.  T
E
L
ismorelipidsolubleandisdistributedwidelyinlipophilictissuessuchasthebrain
 T
E
L
ismetabolisedtotriethylleadwhichisthemajortoxicc
o
m
p
ou
n
dwhichleadstosudden
onsetofvomiting,irritability,headache,ataxia,vertigo,convulsions,psychotic
manifestations,coma,anddeath.
 Mortalityrateisaround25.Evenifrecoveryoccurs,thereisoftenpermanent brain
damage manifesting as mental retardation, cerebral palsy, optic neuropathy,
hyperkinesis,andperiodicconvulsions.

22.  F
E
P
andZ
n
p
levels(>50mcg/100ml)—AnelevatedF
E
P
levelindicatesimpairmentofthehaeme
biosyntheticpathwayandmayresultfromleadpoisoningorirondeficiency.
 Inordertoconfirmwhetheritisduetotheleadpoisoning,theB
L
mustbeestimated
 TodayZ
n
PlevelsaremorecommonlystudiedthanF
E
P
 Urinelevelsofaminolaevulinicacid(ALA)canalsoserveasasensitiveindicatorofleadpoisoning.
 Completebloodcountandperipheralsmear-includelowhaematocritandhaemoglobinvalues,peripheral
smearmayeitherbenormochromicorhypochromic,Basophilicstipplingandmicrocytic.
 Hypochromiaandbasophilicstipplingarestronglysuggestiveofleadintoxication

23.  Bloodleadlevelsreflectrecentexposureorexposureoveraperiodofupto3to5weeks.
 Inindividualswithhighorchronicpastexposure,B
Lusuallyunderrepresentsthetotalbodyburden
becausemostleadisstoredintheboneandmaybefoundatnormallevelsintheblood.
 Therecommendedmethodsofestimatingbloodleadlevel(BL)include
 Atomicabsorptionspectroscopy(AAS)
 Electrothermalatomicabsorptionspectroscopy(EAAS),
 Anodicstrippingvoltammetry(ASV)
 Inductivelycoupledplasmaatomicemissionspectroscopy(ICPAES)
 X-rayfluorescencespectroscopy.
 Fastneutronactivationanalysis(
F
N
A
A
)
 Massspectrometry(MS),andmicrowaveplasmadetection

24.  E
A
A
SandA
S
Varethemethodsofchoice.
 Inrecentyears,ICP-AEShasbecomethetechniqueofchoiceowingtosuperiorspecificityandsensitivity
U
R
I
N
E
 A
L
A
inurine
 Urineleadlevel:Ifthisisabove150mcg/litreitisasignificantfinding,butitis
unfortunatelynotveryreliable
 CalciumdisodiumE
D
T
Amobilisationtest:Thistestisdonemainlyinchildrentofindoutwhetherachild
whoseB
L
isbetween25and41mcg/100m
lwillrespondtochelationtherapywithabriskleaddiuresis..

25.  ChildrenwhoseB
L
ismorethan45mcg/100m
lshouldnotreceivethisprovocativetest.
 A
n8
hourC
a
N
a
2
E
D
T
Achelationprovocativetestisconsideredpositiveiftheleadexcretionratiois
morethan0.6(thoughsomecliniciansuseacut-offof0.5).
 Urineporphyrin
 X-Ray
 Radiography-leadlinesinlongandflatbones.

27.  Treat seizures and coma iftheyoccur.
 Provideadequatefluidstomaintainurineflow(optimally1–2mL/kg/h)butavoid
overhydration,whichmayaggravatecerebraledema
 Patientswithincreasedintracranialpressuremaybenefitfromcorticosteroids(eg,
dexamethasone,10m
g
IV)andmannitol(1–2g/kgIV).

28.  Treatmentwithchelatingagentsdecreasesbloodleadconcentrationsandincreasesurinarylead
excretion.
Severeacutepoisoningwithencephalopathy
 B
A
L
4mg/kgimmediately(inchildren)
 CaNa2E
D
T
A75mg/kg/dayIVinfusion
Severeacutepoisoningwithoutencephalopathy
 B
A
L
12mg/kg/day.
 E
D
T
A5
0mg/kg/day.
Moderate poisoning:
 E
D
T
A
5
0
mg/kg/day
Mild poisoning
 D-Penicillamine3
0mg/kg/day

29. Acute ingestion
 Administeractivatedcharcoal(althoughefficacyisunknown).
 Iflead-containingmaterialisstillvisibleo
nabdominalx-rayafterinitial treatment,
considerwhole-bowelirrigation.
 Considerendoscopicorsurgicalremovalofleadforeignbodiesthatexhibitprolonged
gastrointestinalretention

30.  There is no role for dialysis, hemoperfusion, or repeat-dose charcoal.