Assingment on Heavy Metal Poisoning | Mercury (Element) | Arsenic

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.


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

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

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

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

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

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

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

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

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

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

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

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