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Lead poisoning

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Lead poisoning
SpecialtyEmergency medicine Edit this on Wikidata

Lead poisoning (also known as colica pictonium, saturnism, plumbism, Devon colic, or painter's colic) is a medical condition caused by increased levels of the metal lead in the blood. 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, exposure and direct contact. 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. Lead has also been found in some pool paint—especially those painted by lead-based epoxy paint.[1]

History

Lead was first mined in Asia Minor (today Turkey) about 6500 BC. A 6000- to 8000-year-old lead necklace was found[2] in an ancient city site of Anatolia. Lead's easy workability, low melting point and corrosion-resistance were among its attractions.

Lead toxicity was first recognized as early as 200 B.C. Nicander of Colophon wrote of lead-induced anemia and colic in 250 B.C.[3] Gout, prevalent in affluent Rome, is thought to be the result of lead, or leaded eating and drinking vessels. Lead was used in makeup. Sugar of lead (lead(II) acetate) was used to sweeten wine, and the gout that resulted from this was known as saturnine gout.[4]

Aulus Cornelius Celsus, writing ca. A.D. 30, listed white lead on a list of poisons with antidotes (beside cantharides, hemlock, hyoscyamus, poisoned mushrooms, and a swallowed leech), and claimed it could be remedied by mallow or walnut juice rubbed up in wine.[5][6][7] Despite his awareness of lead's toxicity, citing many contemporary authorities, Celsus recommended its use in a wide range of ointments applied to wounds to stop bleeding and reduce infection or inflammation.[8]

Julius Caesar's engineer, Vitruvius, who also served his successor Caesar Augustus, reported, "Water is much more wholesome from earthenware pipes than from lead pipes. For it seems to be made injurious by lead, because white lead, a pigment base produced by soaking lead in vinegar until a soft paste, is produced from it; and this is said to be harmful to the human body."[9] It should be noted that the prevalence of lead poisoning, at least that caused by drinking water containing lead, in ancient Rome is far less than what is traditionally believed. The hardness of Rome's water caused heavy deposits of calcium carbonate to form on pipes and in turn prevented the lead of the pipes from coming into contact with the water, thus reducing the chance of getting lead poisoning from drinking water.[10]

In 1656 the German physician Samuel Stockhausen recognized dust and fumes containing lead compounds as the specific cause of the diseases, called since ancient Roman times morbi metallici, that were known to afflict miners, smelter workers, potters, and others whose work exposed them to it.[11][12]

In 17th-century Germany, an Ulm physician, Eberhard Gockel,[11] noticed that monks who did not drink wine were healthy, while wine drinkers developed colic. Realizing that the wine-disease symptoms matched those described earlier by Stockhausen, he traced the cause to sugar of lead, made by simmering litharge with vinegar, added to "correct" and preserve the wine.[11] This work resulted in an edict, issued by Eberhard Ludwig, Duke of Württemberg in 1696, specifically banning the adulteration of wines with litharge.[11]

In 18th-century Boston, lead poisoning was fairly frequent on account of the widespread drinking of rum in that city, which was distilled in stills with one component (the "worm") made of lead.[13]

Devon colic was an affliction caused by lead poisoning which was suffered by the cider drinking people of Devon during the 17th and 18th centuries.

Chinese alchemists found that lead could be rendered harmless by soaking it in blood and firing it[citation needed]. When this process was repeated several times it provided a protective coat that lead could not pass. The only notable use of this measure was by martial artists so they could use the heavy metal as weights for training.

Today, most exposure in developed countries is the result of occupational hazards, leaded paint, and leaded gasoline (which continues to be phased out in most countries). Lead poisoning interferes with the normal development of the brain.

The term "lead poisoning" is sometimes used as a euphemism for gunshot wounds, as almost all bullets are mainly composed of lead. Despite this, bullets lodged in the body rarely cause significant levels of lead poisoning.[14] Bullets lodged in the joints are the exception, as they deteriorate and release lead into the body over time.[15]

Symptoms and effects

Lead poisoning can lead to many symptoms and signs which vary based on the extent and duration of lead exposure, however none are pathognomonic. Effects include, but are not limited to:

Neuropathy, learning disabilities and behavior

It has been shown to cause permanently reduced cognitive capacity (intelligence) in children, with apparently no lower threshold to the dose-response relationship (unlike other heavy metals such as mercury).[17]

Lead affects the peripheral and central nervous system. The most common sign of peripheral neuropathy due to chronic lead poisoning is painless wristdrop (weakness of the extensor muscles of hand) which usually develops after many weeks of exposure.

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

A May 2000 study by economic consultant Rick Nevin theorizes that lead exposure explains 65% to 90% of the variation in violent crime rates in the U.S.[18][19] A July 2007 paper by the same author claims to show a strong association between preschool blood lead and subsequent crime rate trends over several decades across nine different countries.[20] These results were discussed in a July 2007 Washington Post article, reviving interest in the subject.[21] Nevin's results reflect peer reviewed findings by Dartmouth political scientist Roger Masters,[22][23] and similar work is being done by other researchers. Amherst economist Jessica Reyes' working paper[24] and Masters' work are both pre-publication and available online.

Blood lead concentrations of 20–40 μg/dL have been associated with decreases in neuro-cognitive function. It was found in a large group of current and former inorganic lead workers in Korea that blood lead levels in the range of 20–50 μg/dL were correlated with neuro-cognitive defects. High current blood lead concentrations were correlated with poorer performance on neuro-cognitive function tests.[25]

Other

  • In humans, lead toxicity sometimes causes the formation of a bluish line along the gums, which is known as the Burton line or "lead line."[26], 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 hypochromasia). However, basophillic stippling is also seen in unrelated conditions, such as megaloblastic anemia caused by vitamin B12 (colbalamin) and folate deficiencies.[27]
  • Chronic lead poisoning can produce a lead hue of the skin with a lividity and pallor.[26]
  • It has been suggested in studies that lead cause elevated blood pressure (hypertension) in adults who are exposed to blood level concentrations <20 μg/dL. In humans, the link between blood lead and blood pressure was influenced by the subject's sex or race. Bone lead concentration was a predictor of hypertension in two different studies. The risk for lead-associated hypertension may be lowered by reducing chronic workplace blood lead concentrations from 20-30 μg/dL to <10 μg/dl.
  • Lead accumulation in bone manifests in radiodense lines at the metaphysis in growing children.[28] The effects of bone lead levels on heart rate variability are stronger in patients with metabolic syndrome. [4]
  • People who have been exposed to higher concentrations of lead may be at a higher risk for cardiac autonomic dysfunction on days where the ozone and fine particles are higher.[29]
  • Lead poisoning inhibits urate excretion and predisposes for gout.[30] [31][32] The condition is then known as saturnine gout.

Biological role

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. Lead is able to bind to and interact with many of the same enzymes as these metals but, due to its differing chemistry, does not properly function as a cofactor, thus interfering with the enzyme's ability to catalyze its normal reaction(s).

Lead is removed from the body extremely slowly (mainly through urine, normally at a rate of 0.5 µmol/L), causing accumulation in the tissues. 95% of the absorbed lead is deposited as a lead phosphate complex in the bones.[33]

Heme synthesis

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. Genetic mutations of ALAD cause the disease porphyria, and while lead poisoning is sometimes mistaken for porphyria the distinction is that lead poisoning usually causes anemia while true porphyria does not.

Lead poisoning also inhibits the enzyme ferrochelatase[34] which catalyzes the joining of protoporphyrin IX and Fe2+ to form heme.

Neurotransmission

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.[35]

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.[36]

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.

Occurrence

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, and from ingestion of lead dust or chips from deteriorating lead-based paints. Although this is less of a problem in countries that no longer have leaded gasoline, leaded soil remains prevalent, raising concerns about the safety of urban agriculture.[37] Lead paint 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 teethe 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.[38] In 2004, seven reporters from The Washington Post discovered high levels of lead in the drinking water in Washington, D.C. The team won an award for investigative reporting for a series of articles about this contamination.[39][40]

Ingestion of metallic lead, such as small lead objects, will lead to an increase in blood lead levels, and possibly death.[41][42][43][44]

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 and from imported toys, such as many made in China. 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.[45]

Lead can leach from leaded china, dishes, and mugs. One TV station found that 30% of dishes of concern that consumers brought in for testing contained lead.[46] (This was not a scientific survey of random plates currently on the market.) Some tableware leaches lead in excess of the FDA or California proposition 65 limits.[47] Rare cases of poisoning traced to dishes exist,[48] but recalls due to lead leaching are rare.[49]

Lead can also migrate into wells and waterways from nearby rifle ranges, if the right conditions exist. The United States Army has been involved in the clean-up of some of their abandoned rifle ranges.

Lead may be taken in through direct contact with mouth, nose, and eyes (mucous membranes); and breaks in the skin.

Ecologists are concerned about the potential for lead to be released into the air, soil, food and water. Lead entering the food chain is generally from ingestion of contaminated feeds. Luckily, little absorbed lead is secreted into milk or deposited into muscle of animals. Toxicities can also arise from animals that ingest waste such as sewage, where this metal can be contained.[50]

Measurement

One measure of lead in the body is the blood lead level (BLL), measured in micrograms of lead per decilitre 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.[51] BLL measures current exposure to lead,but a blood test is available to measure the amount of lead in your blood and to estimate the amount of your recent exposure to lead. Blood tests are commonly used to screen children for lead poisoning. Lead in teeth or bones can be measured by X-ray techniques, but these methods are not widely available. Exposure to lead also can be evaluated by measuring erythrocyte protoporphyrin (EP) in blood samples. EP is a part of red blood cells known to increase when the amount of lead in the blood is high. However, the EP level is not sensitive enough to identify children with elevated blood lead levels below about 25 micrograms per deciliter (μg/dL). These tests usually require special analytical equipment that is not available in a doctor's office. However, your doctor can draw blood samples and send them to appropriate laboratories for analysis. 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.[52] Fecal lead content that is measured over the course of a few days may also be a very accurate way to estimate the overall amount of childhood lead intake. This form of measurement may serve as a useful way to see the extent of oral lead exposure from all the diet and environmental sources of lead.[53]

Exposures and demographics

The average person has less than 10 micrograms per decilitre, 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 mental/cognitive abilities has been noted at very low levels.[54] The levels found today in most people are orders of magnitude greater than that of ancient times. These levels are within an order of magnitude of levels that have resulted in adverse health effects.[55] Blood lead levels once considered safe are now considered hazardous, with no known threshold.[56] Although many people are exposed to lead through household products, workplace, and lead paint, studies show that noncaucasian people and recent immigrants are at a much greater risk for high levels of exposure than whites[57][verification needed]. Low income people often live in rental housing with lead paint, and unless the landlord conducts regular inspections, paint may begin to peel and residents will be exposed to high levels of lead paint dust, thus greatly increasing their chance of lead poisoning.

Pathways

Almost everyone is exposed to environmental lead. Exposure to lead occurs through inhalation, ingestion or occasionally dermal contact. Lead mining and lead smelting are common in many countries, where children and adults can receive substantial lead exposure from sources uncommon today in the U.S. Most countries have phased out use of leaded gasoline since 2007. Lead exposure in the general population (including children) occurs primarily through ingestion, although inhalation also contributes to lead body burden and may be the major contributor for workers in lead-related occupations. Inhalation is the second major pathway of exposure. Almost all inhaled lead is absorbed into the body, whereas from 20% to 70% of ingested lead is absorbed (with children generally absorbing a higher percentage than adults do). Dermal exposure plays a role for exposure to organic lead among workers, but is not considered a significant pathway for the general population, except in areas where leaded gasoline is used. Organic lead from gasoline additives may be absorbed directly through the skin.[58]

14 to 20% of total lead exposure in the United States is attributed to drinking water.[59] This is mainly due to the corrosion of lead from brass water pipes. Lead solder was used in brass pipes until 1988, and until a litigation settlement in 1995, most brass pipes were a 5 to 7% lead alloy. Newer brass water fittings and piping is formed of non-leaded brass, containing 0.25% to 0.5% lead by weight.[60] As of 2005, lead alloy water meters and other parts were still sold. Municipalities have added chemicals to increase the pH and thus reduce the corrositivity of the public water supply. However chloramines, which were adopted as a substitute for chlorine disinfectants due to fewer health concerns, increase corrositivity.[59]

Children

Lead-contaminated household dust is the major source of lead exposure to children in the U.S.[61] A 2006 study in New York City found lead levels in settled outdoor dust, a source of household dust, of 175 to 730 μg/ft2, and noted that these levels exceed the HUD/EPA lead in indoor dust standard of 40 μg/ft2.[62] In 1978 there were 13.5 million children in the United States with elevated blood lead levels (i.e., 10 µg/dl). By 2002, that number had dropped to 310,000 children.[63] The U.S. incurs $43.4 billion annually in the costs of all pediatric environmental disease, with childhood lead poisoning alone accounting for the vast majority of it.[64]

Adults

Although children are at greater risk from lead exposure, adult exposures can also result in harmful health effects. Most adult exposures are occupational and occur in lead-related industries such as lead smelting, refining, and manufacturing industries. One frequent source of lead exposure to adults is home renovation that involves scraping, remodeling, or otherwise disturbing lead-based paint. Adults can also be exposed during certain hobbies and activities where lead is used. Workers may inhale lead dust and lead oxide fumes, as well as eat, drink, and smoke in or near contaminated areas, thereby increasing their probability of lead ingestion. Between 0.5 and 1.5 million US workers are exposed to lead in the workplace (ATSDR, 1999). Other than the developmental effects unique to young children, the health effects experienced by adults from adult exposures are similar to those experienced by children, although the thresholds are generally higher.[65]

Wildlife

Waterfowl poisoned by lead shotgun pellets were first documented in the US in the 1880s. By 1919, the spent lead pellets from waterfowl hunting was positively identified as the source of killing waterfowl.[66] Withstanding legal challenges, by 1991, a federal court order resulted in the US Fish & Wildlife Service enforcement of a US "nation wide" ban on lead shot (pellets).[67] Since the 1970's, steel shot (non-toxic shot) has been used by waterfowl hunters in the US for specified hunting areas. By 1991, all hunting areas nation-wide required non-toxic shot (steel shot or other USFW approved projectiles) for waterfowl hunting.

The California condor has also been affected by lead poisoning. As a scavenger, condors eat carcasses of game shot but not retrieved. Fragments from lead bullets are also ingested leading to increased lead levels. In an effort to protect this endangered species, in areas designated as the California Condor's range the use of projectiles containing lead has been banned to hunt deer, wild pig, elk, pronghorn antelope, coyotes, ground squirrels, and other non-game wildlife.[68]

Regulation

US rules and regulations

"In 1998, the US Government instituted regulations which limit the amount of lead in toys and other consumer products which are expected to be used by infants to 0.06% (or 600 ppm)."[69][70]

Ten µg/dL (micrograms /deciliter) was adopted by the Centers for Disease Control (CDC) in 1991 as an action level for children, an advisory level for environmental and educational intervention, though the agency acknowledges that "Recent studies have suggested possible neurodevelopmental effects concentrations of less than 10 µg/dL."[71] There are requirements that children receiving Medicaid be screened. Most states ask or require primary care physicians and persons in charge of screening programs to report both presumptive and confirmed cases of lead toxicity to the appropriate health agency. This is to ensure abatement of the lead source, education of the patient, and remediation steps are undertaken. In some states, the clinical laboratories performing blood lead testing are required to report cases of lead toxicity.

In 2006 the Lead Poisoning Reduction Act was introduced to protect children from lead poisoning by requiring all non-home-based child care facilities (i.e., Head Start and kindergartens) to be lead-safe within five years.[72]

In early 2008, the watchdog Food and Drug Administration ordered several US retail stores and malls to remove bindi and sindoor from their shelves due to concerns over high lead and other harmful chemical contents.[73]

In October 2008, the U.S. Environmental Protection Agency‎ (EPA) reduced the allowable lead level by a factor of ten to 0.15 micrograms of lead per cubic meter of air (ug/m3).[74] States will have five years to comply with the standards. Tightening the allowable level will primarily affect smelters, iron and steel foundries, and the aviation industry.

Workplace air

The OSHA Lead Standard specifies the permissible exposure limit (PEL) of lead in the workplace, the frequency and extent of medical monitoring, and other responsibilities of the employer. OSHA has set a PEL (enforceable) of lead in workplace air at 50 µg/m3 averaged over an 8-hour workday for workers in general industry. NIOSH at CDC has set a Recommended Exposure Limit (REL) of 50 µg/m3 to be maintained so that worker blood lead remains < 60 µg/dL of whole blood.[75] The ACGIH has set a threshold limit value for a time-weighted average (TLV/TWA) of 50 µg/m3 for lead in workplace air (except for lead arsenate).[76]

The NIOSH Adult Blood Lead Epidemiology and Surveillance (ABLES) program,[77] a state-based surveillance program of laboratory-reported adult blood lead levels works to reduce the rate of adults (age 16 or older) who have blood lead levels of 25 micrograms per deciliter (mcg/dL) or greater.[78]

Lead contaminated soil can pose a risk through direct ingestion, uptake in vegetable gardens, or tracking into homes. Uncontaminated soil contains lead concentrations less than 50 ppm but soil lead levels in many urban areas exceed 200 ppm. (AAP 1993) The EPA's standard for lead in bare soil in play areas is 400 ppm by weight and 1200 ppm for non-play areas. This regulation applies to cleanup projects using federal funds. The soil screening level (SSL) for lead represents a conservative estimate for a level that would be protective of public health in residential soils based on an analysis of the direct ingestion pathway for children.

EPA has set drinking water standards with two levels of protection. The Maximum Contaminant Level Goal is zero. This is the level determined to be safe by toxicological and biomedical considerations, independent of feasibility. EPA's final rule establishes an action level is set at 15 µg/L. The use of lead solder and other lead-containing materials in connecting household plumbing to public water supplies was banned by EPA as of June 1988.

FDA has set a number of action levels (enforceable) and levels of concern for lead in various food items. These levels are based on FDA calculations of the amount of lead a person can consume without ill affect. FDA has set an action level of 0.5 µg/mL for lead in products intended for use by infants and children and has banned the use of lead-soldered food cans.[79]

House paint contained up to 50% lead before 1955. Federal law lowered the amount of lead allowable in paint to 1% in 1971. The CPSC has limited since 1977 the lead in most paints to 0.06% (600 ppm by dry weight). Paint for bridges and marine use may contain greater amounts of lead.[80]

Both the federal government and the state of Massachusetts are considering (as of September 2007) action against lead in children's jewelry.

Less regulated countries

Dermatologists have concluded that the internal effects of lead are dangerous, as it has effects on the central nervous system, kidney and heart. Nevertheless, the emergence of synthetic dye industry has led to a variety of chemical dyes and salts being produced at a cheaper price in India. And the contraband exporting of children's toys and cheap plastics painted with lead paint from Mainland China to other less affluent countries. See 2007 Chinese export recalls.

Lead is commonly incorporated into herbal remedies such as Indian Ayurvedic preparations and preparations of Chinese origin. People who take these herbal remedies can get lead poisoning.

A source of exposure to lead can come from drinking water. This is of particular concern internationally in cities where lead plumbing is still being used. In Australia a problem arises when rain water from roof runoff into tanks is used as potable water. If there is lead contaminates in the roof area or storage tank, the rain water will contain lead. The Australian Drinking Water Guidelines allow a maximum of .01 mg/dL lead in water.[81]

Diagnosis and treatment

Diagnosis

Diagnosis of lead poisoning involves determining the history of exposure, physical findings, and an elevated body burden of lead. Blood lead level analysis may be used to determine the appropriate course of treatment.

Clinical toxicologists are medical specialists in the area of poisoning and may be involved in diagnosis/treatment.

Even though symptoms/signs might not immediately indicate it, high-level exposure acute poisoning would be considered a medical emergency since prompt treatment would start to alleviate any existing problems, may reduce the chance of further problems developing in the short term e.g. delayed encephalopathy, and also reduce the chance of long term damage. In these cases of one-off acute poisoning it is important to carry out blood lead level testing as soon as possible after exposure to accurately gauge the extent of poisoning, since over time the concentration of lead in the blood will reduce as lead is excreted and also further absorbed into the body.

Treatment

In all types of poisoning the source of lead should be identified and exposure to it reduced. Chelation therapy may be administered to reduce not only blood lead levels but also, importantly, overall body burden. U.S. Food and Drug Administration (FDA) approved chelating agents for lead are:

Severe cases of acute poisoning may also require:

Environmental illness

Chelation therapy is also administered by some physicians, especially those who practice in alternative medicine and/or treatment of environmental illness, to patients suffering from illness thought to be related to chronic low-level exposure to heavy metals, including lead. As opposed to acute poisoning, in these cases BLL analysis is not considered an effective test since it doesn't provide information on the body burden of heavy metals. Controversially, hair analysis is sometimes used as a screening test. Commonly though, mobilization testing, also known as challenge or provocation testing, is used to indicate an elevated and mobilizable body burden of heavy metals. This testing involves administering a one-off dose of chelating agent to a patient to mobilize heavy metals from blood, soft tissue and, in some cases, bone. Following this, urine is collected over a pre-defined time period and then analysed by a laboratory for levels of heavy metals, from which overall body burden is inferred. [82] Repeated cycles of chelation therapy treatments and mobilization testing may then be administered until the body burden has fallen to acceptable levels.

In addition to the prescription drugs used in chelation therapy, products classified as dietary supplements are also available to the public. DMSA, although classified only as a drug by the FDA, [83] may be available in some worldwide locations marketed as a supplement. EDTA, an amino acid, can be found as an ingredient in some liquid/pill/suppository supplements. In addition other products exist that may be based on natural ingredients, such as cilantro or chlorella.

Effects of vitamin C and calcium

Vitamin C is not an FDA approved chelating agent and, as such, is not approved as a treatment for cases of lead poisoning in humans. However, an animal study of the efficacy of various chelating agents in treatment of acute lead poisoning showed that vitamin C (ascorbic acid), along with DMSA, CDTA and DMPS increased survival, while EGTA, N-acetyl-L-cysteine (NAC) and various other agents did not.[84] Furthermore, in humans, high serum levels of vitamin C have been associated with a decreased prevalence of elevated blood lead levels[85] and intervention with supplemental vitamin C was shown to markedly decrease lead levels in smokers (mean: 81%). Authors hypothesize, however, that this effect might be due to an inhibition of lead absorption.[86]

There is evidence that calcium supplementation during pregnancy can reduce blood-lead levels in pregnant women. Continual calcium supplementation in postpartum women reduced blood lead levels 15–20% over the coarse of lactation. Calcium may reduce blood-levels by decreasing intestinal absorption of lead or increasing the excretion of lead from circulation in the body which decreases the risk of fetal and infant exposure. The implications of these findings suggest that calcium supplementation should be considered for populations where dietary calcium intake is low.[87]

Due to the reduction of blood lead levels that results from calcium supplementation during pregnancy and lactation, maternal bone re absorption of lead may be suppressed and kept from circulating lead stores throughout maternal bone. High levels of calcium may be needed to counteract the nutrition needs of the developing fetus. This is significant because more than 95% of lead in the body accumulates in the bones. Fetal exposure to lead from the mother may be preventable with the proper nutritional interventions during the reproductive years.[88]

See also

References

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External links

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