Lead poisoning pathophysiology

Revision as of 15:11, 15 August 2018 by Aksiniya (talk | contribs) (→‎Overview)
(diff) ← Older revision | Latest revision (diff) | Newer revision → (diff)
Jump to navigation Jump to search

Lead poisoning Microchapters


Patient Information


Historical Perspective




Differentiating Lead poisoning from other Diseases

Epidemiology and Demographics

Risk Factors


Natural History, Complications and Prognosis


Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings



Echocardiography and Ultrasound

CT scan


Other Imaging Findings

Other Diagnostic Studies


Medical Therapy


Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Lead poisoning pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides


American Roentgen Ray Society Images of Lead poisoning pathophysiology

All Images
Echo & Ultrasound
CT Images

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Lead poisoning pathophysiology

CDC on Lead poisoning pathophysiology

Lead poisoning pathophysiology in the news

Blogs on Lead poisoning pathophysiology

Directions to Hospitals Treating Psoriasis

Risk calculators and risk factors for Lead poisoning pathophysiology

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


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. [1]



  • 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. [2] [3]



  1. [www.atsdr.cdc.com]
  2. Jaffe EK, Martins J, Li J, Kervinen J, Dunbrack RL (2001). "The molecular mechanism of lead inhibition of human porphobilinogen synthase". J Biol Chem. 276 (2): 1531–7. doi:10.1074/jbc.M007663200. PMID 11032836.
  3. Scinicariello F, Murray HE, Moffett DB, Abadin HG, Sexton MJ, Fowler BA (2007). "Lead and delta-aminolevulinic acid dehydratase polymorphism: where does it lead? A meta-analysis". Environ Health Perspect. 115 (1): 35–41. PMC 1797830. PMID 17366816. Check |pmid= value (help).
  4. Wang A, Wang Q, Song Q, Xu J (2009). "[Study of ALAD and VDR gene polymorphisms associated with lead nephrotoxicity susceptibility]". Wei Sheng Yan Jiu. 38 (3): 326–9. PMID 19548578.
  5. Wu S, Yan C, Shen X (2004). "[Molecular genetic susceptibility to lead poisoning]". Wei Sheng Yan Jiu. 33 (2): 226–8, 232. PMID 15209014.
  6. Shaik AP, Jamil K (2008). "A study on the ALAD gene polymorphisms associated with lead exposure". Toxicol Ind Health. 24 (7): 501–6. doi:10.1177/0748233708095770. PMID 19028776.

Template:WH Template:WS