Page "Lead" Paragraph 5

In the human body, lead inhibits porphobilinogen synthase and ferrochelatase, preventing both porphobilinogen formation and the incorporation of iron into protoporphyrin IX, the final step in heme synthesis.

This causes ineffective heme synthesis and subsequent microcytic anemia.

At lower levels, it acts as a calcium analog, interfering with ion channels during nerve conduction.

This is one of the mechanisms by which it interferes with cognition.

Acute lead poisoning is treated using disodium calcium edetate: the calcium chelate of the disodium salt of ethylene-diamine-tetracetic acid ( EDTA ).

This chelating agent has a greater affinity for lead than for calcium and so the lead chelate is formed by exchange.

This is then excreted in the urine leaving behind harmless calcium.

According to the Agency for Toxic Substance and Disease Registry, a small amount of ingested lead ( 1 %) will store itself in bones, and the rest will be excreted by an adult through urine and feces within a few weeks of exposure.

However, only about 32 % of lead will be excreted by a child.