Pb intoxication

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Also known as Plumbism, Colica Pictonum, Saturnism, Decon´s colic or Painter's colic.

Sources of lead intoxication[✎ edit | edit source]

  • Workplaces: abandoned (industrial) lead sites (from mines to garages working with old car batteries), Industries (mining or lead smelting) often have high levels around => ingestion or inhalation, past use of lead in gasoline has contaminated soils (along roadways)
  • Soil: Direct contamination (playing child) or by grown food there
  • Drinking water: lead water pipes (repairs!)
  • Food: Grown on contaminated soil or uptake through leafs, contaminated while handling (e.g. packaging), ceramic table ware, leaded-crystal glassware, cans…
  • Paint: Old paint contaminates soil and houses, detoriating paint becomes dust
  • And traditions like melting lead over a flame to tell your fortune at New Years Eve (German-speaking countries)
  • Organic and Inorganic lead
  • Today: inorganic lead more spread, but…
  • tetra-ethyl-lead (still used as additive in fuel) can be absorbed through the skin (highly lipophilic!)
  • Lead in compact form non-toxic, forms protective layer of lead carbonate (PbCO3 ) in air, but…
  • …consider old window panes and water pipes!

How lead enters he body[✎ edit | edit source]

  • Ingestion: children mainly because of lead paint – lead enters through normal hand-to-mouth activity. As well home remedies may contain lead.
  • Inhalation (all inhaled, but “only” 20-70 % of ingested lead is absorbed!): in old times because of leaded gasoline, nowadays in workers in lead-using industries and in do-it-yourself home renovation
  • Dermal: organic lead can be absorbed through skin (unusual for normal population)

And where it goes to…[✎ edit | edit source]

Half time in blood are days, in soft tissues are weeks and in mineralizing tissue (teeth/bones) 20 - 30 years, which can lead to

  • Endogenous exposure: Pb may be released into bloodstream (for calcium stress because of pregnancy, lactation, osteoporosis or calcium deficiency).
  • toxic to many organs and tissues incl. heart, bones, intestines, kidneys, reproductive & nervous system
  • Influences development of the nervous system (learning/behavior disorders)
  • Symptoms: abdominal pain, confusion, head ache, anemia, irritability and in severe cases: seizures, coma, death

Toxicity Principle[✎ edit | edit source]

Enzymes and Metal Replacement

  • Enzymes are affected, since Pb binds to sulfhydryl groups (–SH)
  • Ability to mimic other metals (cofactors) used in enzymatic reactions, displacing them (calcium, iron and zinc)
  • Eliminates metals in compounds: PbCO3 built into bone instead of CaCO3
  • Influence on heme synthesis (main cause for pathology) leading to anemia…
  • interference with essential enzyme ALAD (delta-aminolevulinic acid dehydratase) needed for heme synthesis (cofactor in hemoglobin)
  • inhibits enzyme ferrochelatase, which catalyzes the joining of protoporphyrin and Fe2+ to form heme.
  • Lead's interference with heme synthesis results in production of zinc protoporphyrin.
  • buildup of heme precursors, such as aminolevulinic acid, may directly or indirectly harm neurons.

Diagnosis[✎ edit | edit source]

Lead concentration leading to
150 µg/l ALAD inhibition
400 µg/l ALA will be found in urine. Coproporphyrin III as well in urine (in severe cases: dark brown coloring). Makes grey-yelloish skin color in chronic lead intoxication.
200-600 µg/l protoporphyrin concentration in erythrocytes increases => basophilic stippling (you can see it in light microscopy!)
500 µg/l (200 µg/l for children) anemia (inhibited heme production) and decrease of erythrocyte life span. Anulocytes (ring-shaped, monoconcave, hypochrome erythrocyte with central white area – less than 1/3 of surface is red) develop

Treatment[✎ edit | edit source]

Treatment with chelating agent, that has greater affinity for lead than for calcium (lead chelate is formed by exchange).

  • Acute oral uptake of toxic amount: irrigation of stomach, administer active carbon to bind organic Pb compounds, and sodium sulfate to change soluble Pb salts into hardly soluble lead sulfate.
  • Chelating agents bind PB (Pb displaces Ca in complex to be disposed by kidney)
  • ethylenediamine-tetraacetic acid (EDTA) – effective mostly extracellular *1
  • D-penicillamine – effective mostly intracellular *1
  • Chronic intoxication: 2,3-Dimercapto-1-propanesulfonic acid (DMPS)
  • 1 Administer both together, ensure drinking lots of water and working diuresis

Links[✎ edit | edit source]

Sources[✎ edit | edit source]

  • THOMAS, Herdegen. Kurzlehrbuch Pharmakologie und Toxikologie. 2nd edition. 2010. ISBN 978-3131422927.