Lead Salts Poisoning

Introduction of Lead Salts

  • Lead is a heavy metal poison.
  • It is the commonest metal involved in chronic poisoning.
  • Elemental lead exists as a highly lustrous, heavy, silvery-grey metal with a cubic crystal structure.
  • It is quite soft and malleable.
  • Lead is a heavy, soft, steel-gray metal that gives off toxic fumes when it is melted.
  • Lead and its salts are very toxic.

Several of its salts occur as variously coloured powders or liquids that includes:

  • Lead Acetate (Sugar of lead and Salt of Saturn)- It is White acicular crystals.
  • Lead Carbonate (White lead Safeeda)- It occurs as White powder.
  • Lead Nitrate – It occurs in the form of crystalline powder.
  • Lead Sulphate –It occurs as White powder.
  • Lead Chromate (Chrome yellow)- It is in Bright yellow powder.
  • Lead Chlorate – It occurs in the White needle shaped crystals form.
  • Lead Iodide – It is bright yellow powder.
  • Lead Sulphide (Surma)- it is occurs in Cubic crystals form.
  • Lead Monoxide (Mudrasang Litharge)- It is in Brick-red scaly mass.
  • Lead Tetraoxide (Sindur Metia sindur)- It occurs in the form of Red lead Scarlet crystalline powder.
  • Lead Tetra-ethyl – It is Heavy, oily, volatile liquid.


  • Automobile exhaust
  • Battery making
  • Glass manufacture
  • Plastic manufacture
  • House paints
  • Steel welding and cutting.
  • Ayurvedic medicines
  • Retained bullets
  • Ink
  • Automobile storage battery casing.
  • Ceramic glazes
  • Lead pipes
  • Silver jewelers workers.
  • Renovation/modernization of old homes.
  • Candle with lead-containing wicks.


► Lead acetate is used in therapeutics.

► Lead carbonate is used in paints.

► Lead oxide is used in glazing of pottery and enamel ware.

► Tetraethyl lead is used in petrol as an antiknock to prevent detonation in internal combustion engines.

► Lead tetroxide is used in vermilion (“sindoor”) applied by married Hindu women.

► Lead sulfide is used as a collyrium (“surma”)

► The various situations in which lead salts are used in chronic occupational, environmental, or domestic exposure.

► It is also used in Lead-acid batteries.

► It is used for making Projectiles for firearms.

► It is also used for making Glass.

Fatal Dose

  • The fatal dose for Lead acetate is 20 gm.
  • The fatal dose for Lead carbonate is 40 gm.
  • The fatal dose for Lead tetra-ethyl is 100 mg/kg

Fatal Period

2 to 3 days

Absorption, metabolism and excretion

● Lead is absorbed from all routes viz. skin, GIT mucosa, Occupational exposure results mainly from inhalation and ingestion.

● Tetraethyl lead can be absorbed rapidly through intact skin.

● After absorption, it is stored in bones as phosphate and carbonate. It is also deposited in liver and kidney.

● Lead is a cumulative poison and its rate of excretion is less than absorption. It is excreted in urine and bile.

Mechanism of Action

  • Lead combines with sulfhydryl enzymes leading to interference with their act and it inhibit cell metabolism.
  • It decreases haeme synthesis by inactivating enzymes required for heme synthesis and causes anemia that includes-
  • Aminolaevulinic acid dehydratase
  • Aminolaevulinic acid synthetase
  • Coproporphyrinogen oxidase
  • Ferrchelatase
  • It causes hemolysis.
  • Lead increases haemolysis as a result of which immature red cells are released into circulation such as reticulocytes and basophilic stippled cells (the result of aggregation of ribonucleic acid due to inhibition of the enzyme pyrimidine5-nucleotidase which normally eliminates degraded RNA).
  • In the CNS, lead causes oedema and has a direct cytotoxic effect leading to decreased nerve conduction, increased psychomotor activity, lower IQ, and behavioural/learning disorders. Children are especially susceptible. The highest brain concentrations of lead are found in hippocampus, cerebellum, cerebral cortex, and medulla.
  • Lead has deleterious effects on the CVS (hypertension and myocarditis), kidney (nephritis) and reproductive organs (infertility).
  • Lead can also decrease uric acid renal excretion, thereby raising blood urate levels and predisposing to gout (saturnine gout). Elevated urinary levels of N-acetyl-3-D-glucosaminidase and beta-2-microglobulin may serve as early markers of renal injury.

Sign and Symptoms

Acute poisoning

  • Metallic taste
  • Vomiting
  • Colicky abdominal pain
  • Constipation
  • Ataxia
  • Apathy
  • Headache
  • Insomnia
  • Paraesthesia
  • Lethargy
  • Drowsiness
  • Acute lead encephalopathy
  • Convulsions
  • Coma

Chronic poisoning

Mild Toxicity (BL 40 to 60 mcg/100 ml)

  • Myalgia
  • Paraesthesia
  • Fatigue
  • Irritability
  • Abdominal discomfort.

Moderate Toxicity (BL 60 to 100 mcg/100 ml)

  • Arthralgia (especially nocturnal)
  • Muscular exhaustibility
  • Tremor
  • Headache
  • Diffuse abdominal pain
  • Anorexia
  • Metallic taste
  • Vomiting
  • Constipation
  • Weight loss
  • Hypertension.

Severe Toxicity (BL more than 100 mcg/100 ml)

● Facial pallor especially around the mouth (circum-oral pallor) is considered as consistent sign of chronic lead poisoning. It is due to vasospasm in addition to anemia.

● Anemia is due to impairment in heme synthesis and is hypochromic and microcytic type anemia. There is reduced erythrocyte life-span.

● Blood are immature red cells in circulation such as reticulocytes and basophilic stippled cells. Basophilic stippling or punctate basophilia means presence of many dark coloured pinhead sized spots in the cytoplasm of red blood cells. The spots are aggregation of ribonucleic acid (RNA) due to inhibition of the enzyme pyrimidine-5’ nucleotidase that normally eliminates degraded RNA.

● Lead line (Burtonian line) a bluish line is present on gums. The line formation is due to lead sulphide. Lead sulphide is formed due to action of hydrogen sulphide gas, liberated from the decomposed food in the mouth, with lead.

● Colic and constipation (dry belly ache) – Colic affects intestine, ureter or uterus. The attack of colic lasts for few minutes and is in form of severe, intermittent cramps. During colic, the abdominal wall is rigid and contracted. Constipation is associated with the colic.

● Lead palsy is a late phenomenon. The extensor muscles are paralyzed causing wrist drop or foot drop. It is motor type of paralysis. The motor paralysis is due to-

● Interference with phosphocreatine metabolism.

● Peripheral neuropathy.

● Lead encephalopathy is more common in children and presents with sudden onset of vomiting, irritability, headache, ataxia, vertigo, convulsions and coma.

● Hypertension

● Arteriosclerotic nephritis

● Amenorrhea

● Sterility

● Abortion.


  • Chelation- The use of calcium chelate of disodium EDTA act as an ion exchanger in which the Ca++ is exchanged for the heavy metal ion and a soluble and stable chelate of lead is formed. This lead chelate is excreted by kidneys as a ring complex.
  • Diazepam for convulsions is administered.
  • Thiamine is also suggested to improve neurological manifestations of lead poisoning.
  • In acute poisoning stomach wash can be done.
  • Calcium gluconate is also effective in lead colic.
  • IV fluids, (maintain specific gravity of urine under 1020).
  • If intracranial pressure is high due to cerebral oedema, administer mannitol or steroids as required (vide supra).

Post mortem finding

  • Pale skin
  • Blue line on gums.
  • Emaciation
  • Lead line on X-ray.
  • GIT – ulceration, hemorrhage with contracted wall.
  • Renal tubular degeneration.
  • Bone marrow hyperplasia.
  • Segmental demyelination of peripheral nerves.
  • Paralyzed muscles are flaccid and show fatty infiltration.
  • Elevated delta-Aminolaevulinic (ALA) levels in postmortem blood.
  • Pathological lesions or changes are sometimes found in kidneys, liver, male gonads, nervous system, blood vessels.

Forensic Examination and Test for Detection

Tests for lead from Blood

● Complete blood count and peripheral smear.

● FEP and Znp levels (>50 mcg/100 ml).

● Blood lead level (BL)—BL can change rapidly in response to lead intake (e.g. ingestion of lead paint chips).

● Methods of estimating blood lead level (BL) includes-

Atomic absorption spectroscopy (AAS)

► Electrothermal atomic absorption spectroscopy (EAAS)

► Anodic stripping voltammetry (ASV)

► Inductively coupled plasma atomic emission spectroscopy (ICPAES)

► X-ray fluorescence spectroscopy.

► Proton-induced x-ray emission (PIXE)

► Fast neutron activation analysis (FNAA)

Mass spectrometry (MS)

► Microwave plasma detection.

Tests for lead from Urine

  • Urine lead level: If this is above 150 mcg /litre it is a significant finding, but it is unfortunately not very reliable.
  • Calcium disodium EDTA mobilisation test : This test is done mainly in children to find out whether a child whose BL is between 25 and 41 mcg/100 ml will respond to chelation therapy with a brisk lead dieresis.
  • Fluorometry

Tests for lead from Bone

  • X-ray fluorescence technique.
  • EDTA chelation provocative test.
  • Atomic absorption analysis.
  • Radiology

Medico Legal Aspects

  • Accidental poisoning may occur in children (pica). It is almost always accidental or inadvertent in nature.
  • Plumbisim due to industrial hazard.
  • Lead is also used to procure criminal abortion
  • It is used as Cattle poisoning also.
  • Lead intake through various food stuffs and beverage.
  • Lead bullet/ missile embedded in person in firearm injury may cause chronic poisoning (plumbisim), however, reported cases are few.
  • Suicide or homicide are rare but have been reported.


  • Dr. K.S. Narayan Reddy. The essential of forensic medicine and toxicology.34th edition.
  • VV Pillay. Modern medical toxicology.4th edition.
  • R.K.Sharma. Concise textbook of forensic medicine and toxicology. 3rd edition.
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