Lead poisoning

Lead poisoning (also known as plumbism, colica pictonium, saturnism, Devon colic, or painter's colic) is a medical condition caused by increased levels of the heavy metal lead in the body. Lead interferes with a variety of body processes and is toxic to many organs and tissues including the heart, bones, intestines, kidneys, and reproductive and nervous systems. It interferes with the development of the nervous system and is therefore particularly toxic to children, causing potentially permanent learning and behavior disorders. Humans have been mining and using this heavy metal for thousands of years, poisoning themselves in the process. Although lead poisoning is one of the oldest known work and environmental hazards, the modern understanding of the small amount of lead necessary to cause harm did not come about until the latter half of the 20th century. No safe threshold for lead exposure has been discovered—that is, there is no known amount of lead that is too small to cause the body harm.

Classification Classically, "lead poisoning" or "lead intoxication" has been defined as exposure to high levels of lead typically associated with severe health effects. Poisoning is a pattern of symptoms that occur with toxic effects from mid to high levels of exposure; toxicity is a wider spectrum of effects, including subclinical ones (those that do not cause symptoms). However, professionals often use "lead poisoning" and "lead toxicity" interchangeably, and official sources do not always restrict the use of "lead poisoning" to refer only to symptomatic effects of lead. The amount of lead in the blood and tissues, as well as the time course of exposure, determine toxicity.   Lead poisoning may be acute (from intense exposure of short duration) or Chronic (from repeat low-level exposure over a prolonged period), but the latter is much more common.

Diagnosis and treatment of lead exposure are based on blood lead level (the amount of lead in the blood), measured in micrograms of lead per deciliter of blood (μg/dL). Lead forms a variety of compounds and exists in the environment in various forms. Features of poisoning differ depending on whether the agent is an organic compound (one that contains carbon), or an inorganic one. Organic lead poisoning is now very rare, due to the fact that countries across the world have phased out the use of organic lead compounds as gasoline additives, but such compounds are still used in industrial settings. Organic lead compounds, which cross the skin and respiratory tract easily, affect the central nervous system predominantly. Exposure routes Lead is a common environmental pollutant. Causes of environmental contamination include industrial use of lead, such as is found in plants that process lead-acid batteries or produce lead wire or pipes, and metal recycling and foundries. Children living near facilities that process lead, such as smelters, have been found to have unusually high blood lead levels.


the half-life of lead in these tissues is measured in weeks for blood. about 35–40% of inhaled lead dust is deposited in the lungs. but little is known about absorption rates in children. Lead may also be harmful to the developing immune system. and eyes (mucous membranes). nose. It is removed from the body very slowly. and its harmful effects are myriad. and people with deficiencies of calcium. Many other tissues store lead. The estimated half-life of lead in bone is 20–30 years. however inorganic lead found in paint. this mechanism 2 . partly due to the re-release of lead from bone. and years for bone. Lead in the bones. and about 95% of that goes into the bloodstream. which allows the lead to be continuously re-introduced into the bloodstream. nails. or iron. and sweat. and bone can introduce lead into the [18] bloodstream long after the initial exposure is gone. hair and nails is bound tightly and not available to other tissues. ingestion or occasionally skin contact. and teeth) are the brain. which was a gasoline additive and is still used in fuels such as aviation fuel. spleen. Lead may be taken in through direct contact with mouth. zinc. pregnant women. The half-life of lead in the blood in men is about 40 days. Children and infants may absorb about 50% of ingested lead. Tetra-ethyl lead. and most lead-containing consumer products is only minimally absorbed through the skin. The main body compartments that store lead are the blood. Of ingested inorganic lead. Also. Lead also interferes with DNA transcription. but it may be longer in children and pregnant women. about 15% is absorbed. but this percentage is higher in children. passes through the skin. Lead has no known physiologically relevant role in the body. mainly through urine. teeth. Smaller amounts of lead are also eliminated through the feces. and is generally thought not to be harmful. and very small amounts in hair. liver. kidneys. and enzymes that maintain the integrity of the cell membrane. whose bones are undergoing remodeling. Anemia may result when the cell membranes of red blood cells become more fragile as the result of damage to their membranes. enzymes that help in the synthesis of vitamin D. causing production of excessive inflammatory proteins. clearance is much slower.Signs and symptoms Pathophysiology Exposure occurs through inhalation. Lead and other heavy metals create reactive radicals which damage cell structures including DNA and cell membranes. food. In adults. bone. and through breaks in the skin. and lungs. and bone. but those with the highest concentrations (other than blood. Lead interferes with metabolism of bones and teeth and alters the permeability of blood vessels and collagen synthesis. months for soft tissues. soft tissues. if lead exposure takes place over years. The main sources of absorption of inorganic lead are from ingestion and inhalation.

or ALAD. the health effects experienced by adults are similar to those in children. Renal system Kidney damage occurs with exposure to high levels of lead. Lead's interference with heme synthesis results in production of zinc protoporphyrin and the development of anemia. Lead exposure has also been associated with a decrease in activity of immune cells such as polymorphonuclear leukocytes. lead exposure decreased the amount of the gene for the receptor in part of the brain.may mean that lead exposure is a risk factor for asthma in children. another enzyme involved in the 2+ formation of heme. Among the essential metals with which lead interacts are calcium. The toxic effect of lead causes nephropathy and may cause Fanconi syndrome. such as aminolevulinic acid. chemicals used by neurons to send signals to other cells. 3 . It interferes with the release of glutamate. especially the nervous system. The targeting of NMDA receptors is thought to be one of the main causes for lead's toxicity to neurons. which is important in the biosynthesis ofheme. a neurotransmitter important in many functions including learning. which may be directly or indirectly harmful to neurons. the cofactor found in hemoglobin. displacing them at the enzymes on which they act. by blocking NMDA receptors. A Johns Hopkins report found that in addition to inhibiting the NMDA receptor. Complications Lead affects every one of the body's organ systems. Ferrochelatase catalyzes the joining of protoporphyrinand Fe to form heme. the kidneys. lead has been found in animal studies to cause programmed cell death in brain cells. In addition. and reproductive systems. Part of lead's toxicity results from its ability to mimic other metals that take part in biological processes. Intrauterine and neonatal lead exposure promote tooth decay. Enzymes The primary cause of lead's toxicity is its interference with a variety of enzymes due to the fact that it binds to sulfhydryl groups found on many enzymes. One of the main causes for the pathology of lead is that it interferes with the activity an essential enzyme called delta-aminolevulinic acid dehydratase. in which the proximal tubular function of the kidney is impaired. although the thresholds are generally higher. which act as cofactors in many enzymatic reactions. immune. iron. in which urate builds up. as have cataracts. Neurons Lead interferes with the release of neurotransmitters. Lead also inhibits the enzyme ferrochelatase. but also the bones and teeth. thus interfering with the enzyme's ability to catalyze its normal reaction or reactions. Lead poisoning inhibits excretion of the waste product urate and causes a predisposition for gout. due to its differing chemistry. Long-term exposure at levels lower than those that cause lead nephropathy have also been reported as nephrotoxic in patients from developed countries that had chronic kidney disease or were at risk because of hypertension or diabetes mellitus. This condition is known as saturnine gout. Lead also interferes with the normal metabolism of calcium in cells and causes it to build up within them. and zinc. Hearing loss and tooth decay have been linked to lead exposure. Lead is able to bind to and interact with many of the same enzymes as these metals but. and evidence suggests that lower levels can damage kidneys as well. Another effect of lead's interference with heme synthesis is the buildup of heme precursors. and the cardiovascular. Aside from the developmental effects unique to young children. does not properly function as a cofactor.

and social engagement. but this evidence is more limited. Increased blood lead level in children has been correlated with decreases in intelligence. reduces numbers of neurons. and children with blood lead concentrations greater than 10 μg/dL are in danger of developmental disabilities. emotional regulation. and death from stroke. short-term memory. when blood lead levels exceed 40 μg/dL. lead interferes with synapse formation in the cerebral cortex. Reduced academic performance has been associated with lead exposure even at blood lead levels lower than 5 μg/dL. In men. and theirmorphology. Between the blood lead levels of 5 and 35 μg/dL. It causes loss of neurons' myelin sheaths. low birth weight. The effect of lead on children's cognitive abilities takes place at very low levels. neurochemical development (including that of neurotransmitters). and decreases neuronal growth. fine motor skills. prematurity. attention. and studies have also found connections between lead exposure and coronary heart disease. therefore children are at greater risk of lead neurotoxicity than adults are. Lead is able to pass through theplacenta and into breast milk. Lead exposure in young children has been linked to learning disabilities. and organization of ion channels. There is apparently no lower threshold to the dose-response relationship (unlike other heavy metals such asmercury). and blood lead levels in mothers and infants are usually similar. and problems with development during childhood. People who have been exposed to higher concentrations of lead may be at a higher risk for cardiac autonomic dysfunction on days when ozone and fine particles are higher. In a child's developing brain.Cardiovascular system Evidence suggests lead exposure is associated with high blood pressure. sperm count is reduced and changes occur in volume of sperm. Nervous system Lead affects the peripheral nervous system (especially motor nerves) and the central nervous system. an IQ decrease of 2–4 points for each μg/dL increase is reported in children. A pregnant woman's elevated blood lead level can lead to miscarriage. High blood lead levels in adults are also associated with decreases in cognitive performance and with psychiatric symptoms such as depression and anxiety. nonverbal reasoning. Peripheral nervous system effects are more prominent in adults and central nervous system effects are more prominent in children. interferes with neurotransmission. reading and arithmetic ability. A fetus may be poisoned in utero if lead from the mother's bones is subsequently mobilized by the changes in metabolism due to pregnancy. Lead poisoning interferes with the normal development of a child's brain and nervous system. their motility. Reproductive system Lead affects both the male and female reproductive systems. 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- 4 . heart rate variability. The brain is the organ most sensitive to lead exposure. Blood lead levels below 10 μg/dL have been reported to be associated with lower IQ and behavior problems such as aggression. increased calcium intake in pregnancy may help mitigate this phenomenon. in proportion with blood lead levels. Lead causes the axons of nerve cells to degenerate and lose their myelin coats.

with a delay of a few weeks. Blood film examination may reveal basophilic stippling of red blood cells (dots in red blood cells visible through a microscope).cognitive defects. Thus EP levels in conjunction with blood lead levels can suggest the time period of exposure. The main tool in diagnosing and assessing the severity of lead poisoning is laboratory analysis of the blood lead level (BLL). Due to this higher threshold for detection and the fact that EP levels also increase in iron deficiency. Lead exposure in children is also correlated with neuropsychiatric disorders such as attention deficit hyperactivity disorder and antisocial behavior. if blood lead levels are high but EP is still normal. 5 . Exposure to lead also can be evaluated by measuring erythrocyte protoporphyrin (EP) in blood samples. impairment of central nervous system function. Diagnosis Diagnosis includes determining the clinical signs and the medical history. as well as the changes normally associated with iron-deficiency anemia (microcytosis and hypochromasia). Countries with the highest air lead levels have also been found to have the highest murder rates. may be involved in diagnosis and treatment. the EP level alone is not sensitive enough to identify elevated blood lead levels below about 35 μg/dL. However. medical specialists in the area of poisoning. However. with inquiry into possible routes of exposure. and possibly permanent. this finding suggests exposure was recent. Clinical toxicologists. such as megaloblastic anemia caused by vitamin B12 (colbalamin) and folate deficiencies. Increases in blood lead levels from about 50 to about 100 μg/dL in adults have been found to be associated with persistent. after adjusting for confounding factors. basophilic stippling is also seen in unrelated conditions. A correlation has also been found between prenatal and early childhood lead exposure and violent crime in adulthood. use of this method for detecting lead exposure has decreased. EP is a part of red blood cells known to increase when the amount of lead in the blood is high. Elevated lead levels in children are correlated with higher scores on aggression and delinquency measures.

water. Prevention measures also exist on national and municipal levels. and viral gastroenteritis in children. Prevention In most cases. especially around the knees. Prevention strategies can be divided into individual (measures taken by a family). air. Regulations exist to limit the amount of lead in paint. Screening is an important method in preventive medicine strategies.Blood lead levels are an indicator mainly of recent or current lead exposure. encephalitis in adults. renal colic. and eliminating the presence of lead-containing objects such as blinds and jewellery in the house. these can be replaced. Lead in bones can be measured noninvasively by X-ray fluorescence. and mental retardation. 6 . preventive medicine (identifying and intervening with high-risk individuals). Another radiographic sign of elevated lead levels is the presence of radiodense lines called lead lines at the metaphysis in the long bones of growing children. Recommendations by health professionals for lowering childhood exposures include banning the use of lead where it is not essential and strengthening regulations that limit the amount of lead in soil. Screening programs exist to test the blood of children at high risk for lead exposure. Guillain-Barré syndrome. These lead lines. abdominal colic. iron deficiency. caused by increased calcification due to disrupted metabolism in the growing bones. household dust. the way to prevent it is to prevent exposure to lead. 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. or adjusting the water's chemistry to prevent corrosion of pipes. subdural hematoma. Lead testing kits are commercially available for detecting the presence of lead in the household. and public health (reducing risk on a population level) . In houses with lead pipes or plumbing solder. Other differential diagnoses in children include constipation. not of total body burden. Conditions that present similarly and must be ruled out in diagnosing lead poisoning include carpal tunnel syndrome. Lead poisoning shares symptoms with other conditions and may be easily missed. lead poisoning is preventable. neoplasms of the central nervous system. discouraging them from putting their hands to their mouths. become wider as the duration of lead exposure increases. X-rays may also reveal lead-containing foreign materials such as paint chips in the gastrointestinal tract. such as those who live near lead-related industries. Recommended steps by individuals to reduce the blood lead levels of children include increasing their frequency of hand washing and their intake of calcium and iron. emotional and behavior disorders. and products. appendicitis. vacuuming frequently. this may be the best measure of cumulative exposure and total body burden. Less permanent but cheaper methods include running water in the morning to flush out the most contaminated water. However this method is not widely available and is mainly used for research rather than routine diagnosis. Fecal lead content that is measured over the course of a few days may also be an accurate way to estimate the overall amount of childhood lead intake.

also known as provocation testing. thus repeated treatments are often necessary. cathartics. Chelation challenge mainly measures the burden of lead in soft tissues. and succimer and d-penicillamine. Treatment of iron. A chelating agent is a molecule with at least two negatively charged groups that allow it to form complexes with metal ions with multiple positive charges. blood lead levels may rise after chelation is stopped because lead is leached into blood from stores in the bone. chelation therapy. When lead-containing materials are present in the gastrointestinal tract (as evidenced by abdominal X-rays). The chelate that is thus formed is nontoxic and can be excreted in the urine. and may not accurately reflect long-term exposure or the amount of lead stored in bone. Mercury poisoning 7 . preventing further exposure. and encephalopathy. use in asymptomatic people with high blood lead levels is more controversial Chelation therapy is of limited value for cases of chronic exposure to low levels of lead. anticonvulsants may be given to control seizures. which are injected. or even surgical removal may be used to eliminate it from the gut and prevent further exposure. for people who have significantly high blood lead levels or who have symptoms of poisoning. When lead exposure has taken place over a long period. such as lead. Lead-containing bullets and shrapnel may also present a threat of further exposure and may need to be surgically removed if they are in or near fluid-filled orsynovial spaces. and treatments to control swelling of the braininclude corticosteroids and mannitol. Chelation therapy is usually stopped when symptoms resolve or when blood lead levels return to premorbid levels. whole bowel irrigation. Chelation challenge. endoscopy. is another part of treatment for lead poisoning. dimercaprol (BAL). If lead encephalopathy is present. While the use of chelation for people with symptoms of lead poisoning is widely supported. Chelation therapy is used in cases of acute lead poisoning. The chelating agents used for treatment of lead poisoning are edetate disodium calcium (CaNa2EDTA). which are administered orally. severe poisoning. for example. from this analysis overall body burden is inferred. Although the technique has been used to determine whether chelation therapy is indicated and to diagnose heavy metal exposure. This testing involves collecting urine before and after administering a one-off dose of chelating agent to mobilize heavy metals into the urine. calcium. treating seizures. Then urine is analyzed by a laboratory for levels of heavy metals.Treatment The mainstays of treatment are removal from the source of lead and. and possibly chelation therapy for people with high blood lead concentrations. Treatment of organic lead poisoning involves removing the lead compound from the skin. Chelating agents can have adverse effects. chelation therapy can lower the body's levels of necessary nutrients like zinc. initially at up to 50 times the normal rate. evidence does not support either of these uses because levels after chelation are not comparable to those in the general population. is used to indicate an elevated and mobilizable body burden of heavy metals including lead. and zinc deficiencies. and is considered for people with blood lead levels above 25 µg/dL. which are associated with increased lead absorption. Chelating agents taken orally can increase the body's absorption of lead through the intestine.

waste disposal. Mercury and its compounds are commonly used in chemical laboratories. although plants and livestock also contain mercury due to bioaccumulation of mercury from soil. An estimated two-thirds of human-generated mercury comes from stationary combustion. inorganic mercury compounds (as salts). including acrodynia (pink disease). Mercury exposure in young children can have severe neurological consequences. human crematoria. Mercury inhibits the formation of myelin. kidney. pig iron and steel production. batteries. mercury production (mostly for batteries). and teeth. Exposure to mercury can occur from breathing contaminated air. Toxic effects include damage to the brain.01% of ingested mercury is absorbed through the intact gastrointestinal tract. HunterRussell syndrome. and adversely affects the mouth. Mercury and many of its chemical compounds. dental clinics. especially organomercury compounds. It damages the central nervous system. from exposure to mercury vapor in mercury amalgam dental restorations. Its zero oxidation state Hg exists as vapor or as liquid metal. and its mercuric state Hg may form either inorganic salts or organomercury compounds. endocrine system. or organomercury compounds. and much remains unknown about the mechanism. There is some evidence that mercury with bronchiectasis and low sperm count). can also be readily absorbed through direct contact with bare. Cases of systemic toxicity from accidental swallowing are rare. and due to biomagnification by ingesting other mercury-containing organisms. Other important human-generated sources include gold production. skin. with natural sources such as volcanoes responsible for the remainder. Elemental mercury Quicksilver (liquid metallic mercury) is poorly absorbed by ingestion and skin contact. all of which can 0 produce toxic effects in high enough doses. Mechanism Mercury is such a highly reactive toxic agent that it is difficult to identify its specific mechanism of damage.kidneys. Animal data indicate that less than 0. and facilities involved in the production of items such as fluorescent light bulbs. the three groups vary in effects. Mercury (chemical symbol Hg) is aheavy metal that occurs in several forms. and explosives. from eating foods containing mercury residues from processing. Human-generated sources such as coal plants emit approximately half of atmospheric mercury.Mercury poisoning (also known as hydrargyria or mercurialism) is a disease caused by exposure to mercury or its compounds. and biomass burning. and lungs. gums. non-ferrous metal production. preventing nerve sheaths from forming properly. Mercury poisoning can result in several diseases. caustic sodaproduction. such as can occur with high-fructose corn syrup. its + 2+ mercurous state Hg exists as inorganic salts. though it may not be true for individuals suffering from ileus. hospitals. Exposure over long periods of time or heavy exposure to mercury vapor can result in brain damage and ultimately death. and Minamata disease. poisoning may predispose to Young's syndrome (men Mercury poisoning's effects partially depend on whether it has been caused by exposure to elemental mercury. mostly of coal. water and atmosphere. for example. and attempted suicide via 8 . or in some cases (such as dimethylmercury) insufficiently protected. after spills of elemental mercury or improper disposal of fluorescent lamps. Mercury and its compounds are particularly toxic to fetuses and infants. Women who have been exposed to mercury in pregnancy have sometimes given birth to children with serious birth defects. cement production. It is hazardous due to its potential to release mercury vapour. and other organs. Causes The consumption of fish is by far the most significant source of ingestion-related mercury exposure in humans. and from improper use or disposal of mercury and mercury-containing objects.

and brain damage. it may take months or even years for the body to eliminate excess mercury. and can cause severe kidney damage. Exposure to large doses at one time can lead to sudden death. Chronic exposure to trace amounts of the compound can lead to mercury buildup in the body over time. thus. such as tuna or swordfish. sometimes ending in coma and death. or passage through the skin. The most dangerous mercury compound. The longest recorded latent period is five months after a single exposure. dimethylmercury. increased saliva. Larger species of fish. ingestion. Contact with eyes can cause burns and brown stains in the eyes. The toxic damage appears to be determined by the peak value of mercury. Ethylmercury is a breakdown product of the antibacteriological agent ethylmercurithiosalicylate. Mercuric cyanide has not been tested on its ability to cause reproductive damage. It is cleared from the blood much more rapidly. can cause death. memory loss. as they can not cross the blood-brain barrier easily. Hg(CN)2 can enter the body via inhalation. reaching high concentrations among populations of some species. mercury salts inflict little neurological damage without continuous or heavy + 2+ exposure. they should be handled with care [19] as they are known to damage developing embryos and decrease fertility in men and women. which has been used as a topical antiseptic and a vaccine preservative (further discussed under Thiomersal below).intravenous injection does not appear to result in systemic toxicity. irritation. As two oxidation states of mercury form salts (Hg and Hg ). or even a latex glove. Though not studied quantitatively. sore gums. mercury salts occur in both mercury(I) (or mercurous) and mercury(II) (mercuric) forms. Contact with skin can cause skin allergy. skin absorption would not be high. It works its way up the food chain through bioaccumulation in the environment. typically paresthesia (a tingling or numbness in the skin). Its characteristics have not been studied as extensively as those of methylmercury. When the first symptom appears. Hg(CN)2 is a particularly toxic mercury compound. loss of appetite. Some mercury vapour is absorbed dermally but uptake by this route is only approximately 1% of that by inhalation. Heating or contact of Hg(CN) 2 with acid or acid mist releases toxic mercury and cyanide vapors that can cause bronchitis with cough and phlegm and/or lung tissue irritation. not the length of the exposure. are usually of greater concern than smaller species. leading to 'shakes' (ex: shaky handwriting). metallic taste. is so toxic that even a few microliters spilled on the skin. Methylmercury is the major source of organic mercury for all individuals. irritability. it is followed rapidly by more severe effects. however. personality changes. Although inorganic mercury compounds (such as Hg(CN)2) have not been shown to be human teratogens. No explanation for this long latent period is known. Mercury(II) salts are usually more toxic than their mercury(I) counterparts because their solubility in water is greater. and long time exposure can affect the peripheral vision. and gray skin color. other latent periods in the range of weeks to months have also been reported. Inhalation of mercuric cyanide irritates the throat and air passages. Organic mercury compounds Compounds of mercury tend to be much more toxic than the element itself. and it is metabolized much more quickly than 9 . Mercury salts primarily affect the gastrointestinal tract and the kidneys. the physical properties of liquid elemental mercury limit its absorption through intact skin and in light of its very low absorption rate from the gastrointestinal tract. they are more readily absorbed from the gastrointestinal tract. Overexposure to mercuric cyanide can lead to kidney damage and/or mercury poisoning. both life-threatening mercury and cyanide poisoning can occur. There is a long latent period between exposure to methylmercury and the appearance of symptoms in adult poisoning cases. Inorganic mercury compounds Mercury occurs inorganically as salts such as mercury(II) chloride. with a half-life of 7 to 10 days. If ingested. and organic compounds of mercury are often extremely toxic and have been implicated in causing brain and liver damage.

and DMPS. but instead relies on simple diffusion to enter the brain. but epidemiological studies have found little evidence that selenium helps to protect against the adverse effects of methylmercury. If the exposure is chronic.    Chelation therapy for acute inorganic mercury poisoning can be done with DMSA. urine levels can be obtained.3-dimercapto-1propanesulfonic acid (DMPS). It is difficult or impossible to interpret urine samples of patients undergoing chelation therapy. Alpha-lipoic acid (ALA) has been shown to be protective against acute mercury poisoning in several mammalian species when it is given soon after exposure. but were removed in 1990 because of cases of toxicity. correct dosage is required. 24-hour collections are more reliable than spot collections. Inorganic ingestion such as mercuric chloride should be approached as the ingestion of any other serious caustic.   Even if the patient has no symptoms or documented history of mercury exposure. In August 2005. diets rich in fish can result in blood mercury concentrations higher than 200 μg/L. as it is given orally.methylmercury. Diagnosis Diagnosis of elemental or inorganic mercury poisoning involves determining the history of exposure. Chelation therapy can be hazardous. and there is no scientific support for chelation therapy as a treatment for autism. which they believe to causeneurological and other disorders. it is not that useful to measure these levels for suspected cases of elemental or inorganic poisoning because of mercury's short half-life in the blood. several studies found no clear clinical benefit from DMSA treatment for poisoning due to mercury vapor. studies in rats have been contradictory. No scientific data supports the claim that the mercury in vaccines causes autism or its symptoms. DPCN. Treatment Identifying and removing the source of the mercury is crucial. Although it has been hypothesized that frequent low dosages of ALA may have potential as a mercury chelator. Immediate chelation therapy is the standard of care for a patient showing symptoms of severe mercury poisoning or the laboratory evidence of a large total mercury load. but have been shown to increase mercury concentrations in the kidneys and the brain. These were used in indoor latex paints for their anti-mildew properties. causing cardiac arrest that killed a five-year-old autistic boy 10 . It probably does not have methylmercury's ability to cross the blood-brain barrier via a transporter. D-penicillamine (DPCN). Decontamination requires removal of clothes. washing skin with soap and water. or dimercaprol (BAL). an incorrect form of EDTA used for chelation therapy resulted in hypocalcemia. Experimental findings have demonstrated an interaction between selenium and methylmercury. 2. a minority of physicians (predominantly those in alternative medicine) use chelation to "rid" the body of mercury. Diagnosis of organic mercury poisoning differs in that whole-blood or hair analysis is more reliable than urinary mercury levels. and has been found to be superior to BAL. DMSA is the most frequently used for severe methylmercury poisoning. Only DMSA is FDA-approved for use in children for treating mercury poisoning. and then use laboratory reports to diagnose the patient with toxic levels of mercury. A common practice is to challenge the patient's body with a chelation agent. as the therapy itself increases mercury levels in the samples. Glutathione and N-acetylcysteine (NAC) are recommended by some physicians. and an elevated body burden of mercury. physical findings. The patient is then advised to undergo further chelation. and flushing the eyes with saline solution as needed. as inappropriate dosages increase toxicity. collect urine samples. However. often no pre-chelation urine sample is collected for comparison. has fewer side effects. Although whole blood mercury concentrations are typically less than 6 μg/L. No chelator for methylmercury or ethylmercury is approved by the FDA. Other exposure sources of organic mercury include phenylmercuric acetate and phenylmercuric nitrate.

Pathophysiology 11 . including cutaneous hyperpigmentation. Moreover. prolonged qt interval. which may affect the structure and function of cardiovascular system. Further. tachycardia and hypertension with mild headaches and lightheadedness if chronic and untreated will result in damage to the kidneys. leading to death from multisystem organ failure. tenesmus. leading to reduction in the generation and bioavailability of nitric oxide. Due to the regular appearance of Arsenic in public drinking water supplies. Arsenic is a ubiquitous element present in drinking water. neuropathy. such as pyruvate and alpha-ketoglutarate dehydrogenase. it is likely that Arsenic plays a part in about thirty percent of total all cause mortality in America. but by one of arsenics compounds. and its exposure is associated with various cardiovascular disorders. the chronic arsenic exposure induces high oxidative stress. Toxicity The toxicity of arsenic and its compounds is not highly variable. clammy sweats. Because of this. lividity of the extremities. the arsenic exposure has been noted to induce atherosclerosis by increasing the platelet aggregation and reducing fibrinolysis. These diseases are all related to the alteration of voltage dependent potassium channels. arsenic exposure may cause arrhythmia by increasing the QT interval and accelerating the cellular calcium overload. eyes red and sparkling. brain or even death. especially arsenic trioxide. hoarseness and difficulty of speech. disrupting cellular electrolytic function resulting in neurological disturbances. countenance collapsed. diarrhea. Arsenic poisoning can lead to a variety of problems by its effect on voltage dependent potassium channels. Some of these symptoms may be absent where the poisoning results from inhalation. vomiting. Chronic exposure to inorganic arsenic may lead to Hypertension. Symptomatic arsenic poisoning starts with changes in respiration. as of arseniuretted hydrogen. delirium. Arsenic exposure plays a key role in the pathogenesis of vascular endothelial dysfunction as it inactivates endothelial nitric oxide synthase. Arsenic is suspiciously related to at least the first four leading causes of death in the united states: Heart disease (hypertension related cardiovascular). death. sometimes excoriation of the anus. diabetes. Symptoms include violent stomach pains in the region of the bowels. It particularly affects potassium dependent voltage channels. urinary organs occasionally affected with violent burning pains and suppression. Arsenic prevalence in the water has been related to the occurrence of hypertension. Cancer. involuntary muscular dysfunction (including incontinence). central nervous system dysfunction and death. which is approximately 500 times more toxic than pure arsenic. Most reported arsenic poisonings are not caused by elemental arsenic. tenderness and pressure. The chronic exposure to arsenic upregulates the expression of tumor necrosis factor-α. Research has shown that arsenites (trivalent forms) have a higher acute toxicity than arsenates (pentavalent forms). vascular cell adhesion molecule and vascular endothelial growth factor to induce cardiovascular pathogenesis. retching. substrates before the dehydrogenase steps accumulate. It primarily inhibits enzymes that require lipoic acid as a cofactor. erectile dysfunction and related conditions. sometimes streaked with blood. thirst. excessive saliva production. obesity and any other condition related to the altered role of intercellular voltage dependent potassium channels. Organic forms appear to have a lower toxicity than inorganic forms of arsenic. the matter vomited. such as pyruvate (and lactate). heart. depression. Diabetes is also related to alteration of voltage dependent potassium channels due in part to the function of insulin and potassium in the cellular metabolism of glucose. greenish or yellowish. convulsions and cramps. Stroke (cerebrovascular diseases)and Chronic lower respiratory diseases. interleukin-1. sense of dryness and tightness in the throat. In addition. The acute minimal lethal dose of arsenic in adults is estimated to be 70 to 200 mg or 1 mg/kg/day.Arsenic poisoning Arsenic poisoning kills by allosteric inhibition of essential metabolic enzymes.

00017 mg/L (0. among workers involved in the production or application of pesticides containing organic arsenicals. At the level of the citric acid cycle. These metabolic interferences lead to death from multi-system organ failure. Remains of arsenic in nails (which show as white spots and lines) and hair can be detected years after the exposure. Humans are exposed to arsenic through air. Arsenic was also found in wine if arsenic pesticides are used in the vineyard. and ATP synthesis. most of a single. This may occur due to arsenic contamination of groundwater. A post mortem reveals brick red colored mucosa.01 mg/L (10ppb) of arsenic in drinking water. thus inhibiting energy-linked reduction of NAD+. and poultry). Inorganic arsenic is also found in coke oven emissions associated with the smelter industry. probably from necrotic cell death. The most important side-effect is hypertension. poultry is usually the largest source of food based arsenic injestion due to usage of certain antibiotics in chicken feed. fish. Occupational exposure to arsenic may occur with copper or lead smelting and wood treatment. not apoptosis. Arsenicosis: chronic arsenic poisoning from drinking water Chronic arsenic poisoning results from drinking water with arsenic over a long period of time. 12 . Dimercaprol and dimercaptosuccinic acid are chelating agents which sequester the arsenic away from blood proteins and are used in treating acute arsenic poisoning. Treatment Chemical and synthetic methods are now used to treat arsenic poisoning. and food (meat. low-level dose is excreted within a few days after consuming any form of inorganic arsenic. Arsenic also disrupts ATP production through several mechanisms. Although arsenic causes toxicity. and electronic semiconductor manufacturing. it can also play a protective role. Occupational Exposures Industries that use inorganic arsenic and its compounds include wood preservation. widely distributed and excreted in urine. This recommendation was established based on the limit of detection of available testing equipment at the time of publication of the WHO water quality guidelines. The World Health Organization recommends a limit of 0. glass production. Hydrogen peroxide production is also increased. due to severe hemorrhage. at the same time. drinking water. Dimercaprol is considerably more toxic than succimer. Arsenic is well absorbed by oral and inhalation routes. More recent findings show that consumption of water with levels as low as 0.17ppb) over long periods of time can lead to arsenicosis. mitochondrial respiration. nonferrous metal alloys.Tissue culture studies have shown that arsenic blocks both IKr and Iks channels and. arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation. activates IK-ATP channels. which might form reactive oxygen species and oxidative stress.

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