Lead poisoning pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aksiniya K. Stevasarova, MD

Overview

Lead poisoning is a medical condition, also known as saturnism, plumbism, or painter's colic caused by increased blood lead levels. Lead may cause irreversible neurological damage as well as renal disease, cardiovascular effects, and reproductive toxicity.

Humans have been mining and using this heavy metal for thousands of years, poisoning themselves in the process due to accumulation and exposure. These dangers have long been known, though the modern understanding of their full extent and the small amount of lead necessary to produce them is relatively recent; blood lead levels once considered safe are now considered hazardous, with no known threshold. Reducing these hazards requires both individual actions and public policy regulations.

Pathophysiology

Pathogenesis

• Lead has no known physiologically relevant role in the body.
• The toxicity of lead comes from its ability to mimic other biologically important metals, most notably calcium, iron and zinc which act as cofactors in many enzymatic reactions.
• Following ingestion, lead is able to bind to and interact with many of the same enzymes as these are metals, but due to its differing chemistry, does not properly function as a co-factor, thus interfering with the enzyme's ability to catalyze its normal reaction(s).
• Lead toxicity symptoms arise are thought to occur by interfering with an essential enzyme delta-AminoLevulinic Acid Dehydratase, or ALAD. ALAD is a zinc-binding protein which is important in the biosynthesis of heme, the co-factor found in hemoglobin. Lead poisoning also inhibits the enzyme ferrochelatase which catalyzes the joining of protoporphyrin IX and Fe2+ to form Heme.