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Lead poisoning
ICD-10 T56.0
ICD-9 984.9
OMIM {{{OMIM}}}
DiseasesDB {{{DiseasesDB}}}
MedlinePlus {{{MedlinePlus}}}
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MeSH {{{MeshNumber}}}


Lead poisoning is a medical condition, also known as saturnism, plumbism or painter's colic, caused by increased levels of Lead in the blood.


Symptoms and effectsEdit

The symptoms of chronic lead poisoning include neurological problems, such as reduced IQ, or nausea, abdominal pain, irritability, insomnia, metal taste in oral cavity, excess lethargy or hyperactivity, headache and, in extreme cases, seizure and coma. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. Other associated effects are anemia, kidney problems, and reproductive problems.

In humans, lead toxicity sometimes causes the formation of a bluish line along the gums, which is known as the "Burton's line", although this is very uncommon in young children. Blood film examination may reveal "basophilic stippling" of red blood cells, as well as the changes normally associated with iron deficiency anemia (microcytosis and hypochromia).

A direct link between early lead exposure and extreme learning disability has been confirmed by multiple researchers and child advocacy groups.

Biological roleEdit

Lead has no known biological role in the body. The toxicity comes from its ability to mimic other biologically important metals, the most notable of which are calcium, iron and zinc. Lead is able to bind to and interact with the same proteins and molecules as these metals, but after displacement, those molecules function differently and fail to carry out the same reactions, such as in producing enzymes necessary for certain biological processes.

Most lead poisoning symptoms 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 cofactor found in hemoglobin. Lead poisoning also inhibits the enzyme ferrochelatase which catalyzes the joining of protoporphyrin IX and Fe2+ to form a Heme. Genetic mutations of ALAD cause the disease porphyria, a disease which was highlighted in the movie The Madness of King George. Lead poisoning is sometimes mistaken for porphyria but the distinction is that lead poisoning usually causes anemia while true porphyria does not.

An article on Lead Encephalopathy on Emedicine states:

Lead also interferes with excitatory neurotransmission by glutamate, which is the transmitter at more than half the synapses in the brain and is critical for learning. The glutamate receptor thought to be associated with neuronal development and plasticity is the N-methyl-D-aspartate (NMDA) receptor, which is blocked selectively by lead. This disrupts long-term potentiation, which compromises the permanent retention of newly learned information.[1]

The January 2004 edition of Scientific American magazine contained an article on Schizophrenia that said the latest research:

... implies that their brain circuits reliant on NMDA receptors are out of kilter. If reduced NMDA receptor activity prompts schizophrenia's symptoms, what then causes this reduction? The answer still remains unclear.

However, a Johns Hopkins report by Tomas Guilarte stated:

It has been known for some time that lead is a potent inhibitor of the NMDA receptor, a protein known to play an important role in brain development and cognition. In this study we demonstrate that lead exposure decreased the amount of NMDA receptor gene and protein in a part of the brain called the hippocampus.[2]

Ezra Susser and his colleagues at Columbia University in New York followed 12,000 children born in Oakland, California, between 1959 and 1966, whose mothers had given samples of blood serum while they were pregnant, which were frozen and stored for later analysis. They found that children who had been exposed to high levels of lead in the womb were more than twice as likely to go on to develop schizophrenia. Their research was presented at the 2004 annual meeting of the American Association for the Advancement of Science in Seattle, Washington.

OccurrenceEdit

Outside of occupational hazards, the majority of lead poisoning occurs in children under age twelve. The main sources of poisoning are from ingestion of lead contaminated soil (this is less of a problem in countries that no longer have leaded gasoline) and from ingestion of lead dust or chips from deteriorating lead-based paints. This is particularly a problem in older houses where the sweet-tasting lead paint is likely to chip, but deteriorating lead-based paint can also powder and be inhaled. Small children also tend to teeth and suck on painted windowsills as they look outside. In most American states, landlords and those selling such houses are required to inform the potential residents of the danger.

Lead has also been found in drinking water. It can come from plumbing and fixtures that are either made of lead or have trace amounts of lead in them.[3] Exposure to lead may also come from bullet fragments in game meat hunted with lead bullets.

Lead can also be found in some imported cosmetics such as Kohl, from the Middle East, India, Pakistan, and some parts of Africa, and Surma from India. There are also risks of elevated blood lead levels caused by folk remedies like Azarcon which contains 95 percent lead and is used to "cure" empacho. For more information about less common causes of elevated blood lead levels, see footnote.[4]

MeasurementEdit

One measure of lead in the body is the blood lead level (BLL), measured in micrograms of lead per deciliter of blood (μg/dL). Nearly everyone has a measurable BLL. The Centers for Disease Control and Prevention (CDC) states that a BLL of 10 μg/dL or above is a cause for concern. However, lead can impair development even at BLLs below 10 μg/dL.[5] However, BLL measures current exposure to lead, but lead may also be incorporated into bone from prior exposures that will not show in BLLs until this bone-lead becomes "mobilized" through pregnancy or fracture healing. A fetus can be poisoned in utero if its mother had high bone-lead from either childhood exposure or a later occupational or other exposure that is subsequently mobilized by the fetal need for calcium. K-fluorescent X-ray metering can measure bone-lead.

The average person has less than 10 micrograms per deciliter, or 100 parts per billion, ppb, of lead in their blood. People who have been exposed to an unusual amount of lead will have blood lead levels higher than 200 ppb—most clinical symptoms of lead poisoning begin at around 100 ppb. The effect on children's IQ has been noted at very low levels.[6]

TreatmentEdit

Although the most important part of treating lead poisoning is decreasing exposure to lead, there are some forms of chelation therapy that can be used to reduce existing BLL levels:

Additionally, vitamin C (ascorbic acid), is also thought to act as a weak (according to some sources) chelating agent,[7] though high serum levels of vitamin C have been associated with a decreased prevalence of elevated blood lead levels.[8]

There are also homeopathic remedies that purport to cure lead poisoning. Asa Herschoff, MD claims that Alumina helps antidote and eliminate lead from the body, and can help mental confusion, memory loss, dullness, lethargy and loss of identity, as well as high blood pressure and kidney disease.[How to reference and link to summary or text] Causticum is also a general antidote, particularly indicated for nerve paralysis and urinary weakness.

Famous cases of lead poisoning Edit

See alsoEdit

ReferencesEdit

  1. http://www.emedicine.com/neuro/topic185.htm
  2. http://www.jhsph.edu/publichealthnews/press_releases/PR_2000/lead_change.html
  3. http://www.waterwebster.com/WashingtonD.C.lead.htm
  4. http://www.cdc.gov/nceh/lead/CaseManagement/caseManage_main.htm
  5. http://www.toxicologysource.com/tox-med/lead/braininjury.html
  6. [1]
  7. Llobet JM, Domingo JL, Paternain JL, Corbella J (1990). Treatment of acute lead intoxication. A quantitative comparison of a number of chelating agents. Arch Environ Contam Toxicol 19 (2): 185-9. PMID 2322019.
  8. Simon JA, Hudes ES (1999). Relationship of ascorbic acid to blood lead levels. JAMA 281 (24): 2289-93. PMID 10386552.
  9. http://goya.unizar.es/InfoGoya/Life/Caracter.html
  10. http://gfhandel.org/frosch.htm
  11. Franklin Saga Deaths: A Mystery Solved? National Geographic Magazine, Vol 178, No 3, Sep 1990

External linksEdit


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