User:GeliMedi/Sandbox
From WikiLectures
PB Intoxication[edit | edit source]
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 of 150 µg/l: ALAD inhibition
- lead concentration of 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.
- lead concentration of 200-600 µg/l: protoporphyrin concentration in erythrocytes increases => basophilic stippling (you can see it in light microscopy!)
- lead concentration of 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
by Angelika Dripke
Sources Source: http://www.atsdr.cdc.gov/csem/csem.asp?csem=7&po=8 Source: http://en.wikipedia.org/wiki/Lead_poisoning#Pathophysiology Source: http://en.wikipedia.org/wiki/Lead#Biochemistry_of_poisoning Source: [Thieme] Kurzlehrbuch Pharmakologie und Toxikologie, Herdegen, 2.2010