Question:

Is lead poisoning curable?

Answer:

Lead poisoning can be treated, but prevention is best. Once lead is in the body there may already be permanent damage. Although not completely curable, lead poisoning is completely preventable through education and environmental interventions.

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A series of lead poisonings in Zamfara State, Nigeria, led to the deaths of at least 163 people between March and June 2010, including 111 children. Health ministry figures state the discovery of 355 cases, with 46 percent proving fatal. An annual immunization programme in Northern Nigeria led to the discovery of a high number of child deaths in the area. An investigation showed that they had been digging for gold at the times of their deaths, in an area where lead is prevalent. It was thought by the villagers that all the children had contracted malaria but Médecins Sans Frontières found unusually high levels of lead in the blood during tests. The BBC suggested the contamination of water may have contributed to the high mortality rate. Blacksmith Institute was called in by the Nigerian authorities to assist in the removal of toxic lead. It is thought that the poisonings were caused by the illegal extraction of ore by villagers, who take crushed rock home with them to extract. This results in the soil being contaminated from lead which then poisons people through hand-to-mouth contamination. Others have been contaminated by contact with contaminated tools and water. In an effort to halt the epidemic the authorities are clamping down on illegal mining and carrying out a clean-up of the area. The number of cases has fallen since April, when illegal mining in the area was halted and some of the residents were evacuated. Education on health and the dangers of lead mining is also being given to local people. It is hoped that the clean-up can be completed prior to the start of the rainy season in July, which will spread contaminants, though it is being hampered by the remoteness of the villages and Muslim restrictions preventing men from entering some compounds. Those who died came from several villages. Five villages in the Local Government Areas of Anka and Bungudu were affected. Two treatment camps were established by health authorities to deal with the crisis. The World Health Organization, Médecins Sans Frontières and Blacksmith Institute assisted with the epidemic. Federal health ministry epidemiologist Henry Akpan said: "We are working with the state ministry of health to give health education and create enlightenment on the dangers of illegal mining". Nigeria's chief epidemiologist Dr. Henry Akpan announced the discovery of the epidemic on 4 June 2010. Blacksmith has been removing toxic lead from houses and compounds in the villages so that surviving children returning from treatment will not be re-exposed to toxic lead in their homes.
The American Association of Poison Control Centers (AAPCC) is a national voluntary health organization founded in 1958 that represents the nation’s 57 poison centers. The AAPCC supports poison centers in their public health mission to prevent poisonings, provide education, conduct scientific research and treat individuals exposed to poisoning from medications, environmental events, plants, animals, and household products or toxins. The AAPCC also supports the efforts of poison centers and interested individuals to reduce morbidity and mortality from unintentional poisonings. The AAPCC sets standards for poison center operations and certifies specialists in poison information who are available 24/7 to respond to public, health-care provider and emergency medical service personnel requests for assistance. In addition, the AAPCC maintains the National Poison Data System, the only poison information and surveillance database in the United States. United States poison centers compose a remarkable nationwide medical calls system. A single toll-free telephone number immediately connects a caller to a specialist in poison information anywhere in the U.S. at any time, day or night. A board-certified toxicologist can be reached within a few moments to provide confidential, expert medical advice to people who have been exposed to a poison. This extraordinary system is maintained by the voluntary cooperation of the 57 member organizations of the AAPCC. The 24-hour national toll-free Poison Help line provides immediate poison information and emergency instructions to all callers regardless of health insurance, immigration status, or language preference from any U.S. telephone or cell phone. Calls are answered by physicians, nurses and pharmacists with highly specialized training in poison management. Poison center services are accessible to all populations, including under-served and undocumented groups, those speaking one of 150 languages and those utilizing telecommunication devices for the hearing impaired (TDD/TTY). More than 70 percent of all cases received by poison centers can be safely and effectively treated at home, without need for further medical care. Substantial cost savings have been attributed to poison center reductions in unnecessary emergency department (ED) care through accurate assessment and triage of poisoning exposures. The public health and cost benefits from poison center pre-hospital management of patients not needing ED visits favorably impacts the self-pay or copaying general public, the health-care institution supporting the costs of indigent care, the commercial insurance companies and governmental health-care funding agencies. Poison centers assess and manage more than 70 percent of poison exposures over the phone, eliminating the need for callers to seek further medical care. This reduction in medically unnecessary ED visits decreases hospital overcrowding and minimizes unnecessary ambulance runs, freeing critical emergency staff to handle true emergencies more effectively. The AAPCC owns and manages a large database of information from all poison exposure and information case phone calls to all poison centers across the country. It is the only near real-time, comprehensive poisoning surveillance database in the United States. NPDS holds more than 50 million poison exposure case records, with more than 2 million new records added each year. It is also a robust and modern system – holding technical medical information that is searchable in many ways. NPDS contains exposure cases dating back to 1985. Today, information and exposure case data is continually uploaded to NPDS from all the poison centers in near “real time.” NPDS can: Key regulatory agencies that rely on NPDS data: NPDS data is also frequently used by pharmaceutical manufacturers.
Lead poisoning (also known as plumbism, colica Pictonum, saturnism, Devon colic, or painter's colic) is a medical condition in humans and other vertebrates 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. Symptoms include abdominal pain, confusion, headache, anemia, irritability, and in severe cases seizures, coma, and death. Routes of exposure to lead include contaminated air, water, soil, food, and consumer products. Occupational exposure is a common cause of lead poisoning in adults. According to estimates made by the National Institute of Occupational Safety and Health (NIOSH), more than 3 million workers in the United States are potentially exposed to lead in the workplace. One of the largest threats to children is lead paint that exists in many homes, especially older ones; thus children in older housing with chipping paint or lead dust from moveable window frames with lead paint are at greater risk. Prevention of lead exposure can range from individual efforts (e.g. removing lead-containing items such as piping or blinds from the home) to nationwide policies (e.g. laws that ban lead in products, reduce allowable levels in water or soil, or provide for cleanup and mitigation of contaminated soil, etc.). Elevated lead in the body can be detected by the presence of changes in blood cells visible with a microscope and dense lines in the bones of children seen on X-ray. However, the main tool for diagnosis is measurement of the blood lead level. When blood lead levels are recorded, the results indicate how much lead is circulating within the blood stream, not the amount being stored in the body. There are two units for reporting blood lead level, either micrograms per deciliter (µg/dl), or micrograms per 100 grams (µg/100 g) of whole blood, which are numerically equivalent. The Centers for Disease Control (US) has set the standard elevated blood lead level for adults to be 10 (µg/dl) of the whole blood. For children however, the number is set much lower at 5 (µg/dl) of blood as of 2012 down from a previous 10 (µg/dl). Children are especially prone to the health effects of lead and as a result, blood lead levels must be set lower and closely monitored if contamination is possible. The major treatments are removal of the source of lead and chelation therapy (administration of agents that bind lead so it can be excreted). 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. 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). The US Centers for Disease Control and Prevention and the World Health Organization state that a blood lead level of 10 μg/dL or above is a cause for concern; however, lead may impair development and have harmful health effects even at lower levels, and there is no known safe exposure level. Authorities such as the American Academy of Pediatrics define lead poisoning as blood lead levels higher than 10 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, because 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. Lead poisoning can cause a variety of symptoms and signs which vary depending on the individual and the duration of lead exposure. Symptoms are nonspecific and may be subtle, and someone with elevated lead levels may have no symptoms. Symptoms usually develop over weeks to months as lead builds up in the body during a chronic exposure, but acute symptoms from brief, intense exposures also occur. Symptoms from exposure to organic lead, which is probably more toxic than inorganic lead due to its lipid solubility, occur rapidly. Poisoning by organic lead compounds has symptoms predominantly in the central nervous system, such as insomnia, delirium, cognitive deficits, tremor, hallucinations, and convulsions. Symptoms may be different in adults and children; the main symptoms in adults are headache, abdominal pain, memory loss, kidney failure, male reproductive problems, and weakness, pain, or tingling in the extremities. Early symptoms of lead poisoning in adults are commonly nonspecific and include depression, loss of appetite, intermittent abdominal pain, nausea, diarrhea, constipation, and muscle pain. Other early signs in adults include malaise, fatigue, decreased libido, and problems with sleep. An unusual taste in the mouth and personality changes are also early signs. In adults, symptoms can occur at levels above 40 μg/dL, but are more likely to occur only above 50–60 μg/dL. Symptoms begin to appear in children generally at around 60 μg/dL. However, the lead levels at which symptoms appear vary widely depending on unknown characteristics of each individual. At blood lead levels between 25 and 60 μg/dL, neuropsychiatric effects such as delayed reaction times, irritability, and difficulty concentrating, as well as slowed motor nerve conduction and headache can occur. Anemia may appear at blood lead levels higher than 50 μg/dL. In adults, Abdominal colic, involving paroxysms of pain, may appear at blood lead levels greater than 80 μg/dL. Signs that occur in adults at blood lead levels exceeding 100 μg/dL include wrist drop and foot drop, and signs of encephalopathy (a condition characterized by brain swelling), such as those that accompany increased pressure within the skull, delirium, coma, seizures, and headache. In children, signs of encephalopathy such as bizarre behavior, discoordination, and apathy occur at lead levels exceeding 70 μg/dL. For both adults and children, it is rare to be asymptomatic if blood lead levels exceed 100 μg/dL. In acute poisoning, typical neurological signs are pain, muscle weakness, paraesthesia, and, rarely, symptoms associated with encephalitis. Abdominal pain, nausea, vomiting, diarrhea, and constipation are other acute symptoms. Lead's effects on the mouth include astringency and a metallic taste. Gastrointestinal problems, such as constipation, diarrhea, poor appetite, or weight loss, are common in acute poisoning. Absorption of large amounts of lead over a short time can cause shock (insufficient fluid in the circulatory system) due to loss of water from the gastrointestinal tract. Hemolysis (the rupture of red blood cells) due to acute poisoning can cause anemia and hemoglobin in the urine. Damage to kidneys can cause changes in urination such as decreased urine output. People who survive acute poisoning often go on to display symptoms of chronic poisoning. Chronic poisoning usually presents with symptoms affecting multiple systems, but is associated with three main types of symptoms: gastrointestinal, neuromuscular, and neurological. Central nervous system and neuromuscular symptoms usually result from intense exposure, while gastrointestinal symptoms usually result from exposure over longer periods. Signs of chronic exposure include loss of short-term memory or concentration, depression, nausea, abdominal pain, loss of coordination, and numbness and tingling in the extremities. Fatigue, problems with sleep, headaches, stupor, slurred speech, and anemia are also found in chronic lead poisoning. A "lead hue" of the skin with pallor is another feature. A blue line along the gum, with bluish black edging to the teeth, known as Burton line is another indication of chronic lead poisoning. Children with chronic poisoning may refuse to play or may have hyperkinetic or aggressive behavior disorders. A fetus developing in the womb of a woman who has elevated blood lead level is also susceptible to lead poisoning, and is at greater risk of being born prematurely or with a low birth weight. Children are more at risk for lead poisoning because their smaller bodies are in a continuous state of growth and development. Lead is absorbed at a faster rate compared to adults, which causes more physical harm than to older people. Furthermore, children, especially as they are learning to crawl and walk, are constantly on the floor and therefore more prone to ingesting and inhaling dust that is contaminated with lead. The classic signs and symptoms in children are loss of appetite, abdominal pain, vomiting, weight loss, constipation, anemia, kidney failure, irritability, lethargy, learning disabilities, and behavioral problems. Slow development of normal childhood behaviors, such as talking and use of words, and permanent mental retardation are both commonly seen. Lead is a common environmental pollutant. Causes of environmental contamination include industrial use of lead, such as is found in facilities 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 lead smelters, have been found to have unusually high blood lead levels. In August 2009, parents rioted in China after lead poisoning was found in nearly 2000 children living near zinc and manganese smelters. Lead exposure can occur from contact with lead in air, household dust, soil, water, and commercial products. In adults, occupational exposure is the main cause of lead poisoning. People can be exposed when working in facilities that produce a variety of lead-containing products; these include radiation shields, ammunition, certain surgical equipment, developing dental x-ray films prior to digital x-rays (each film packet had a lead liner to prevent the radiation from going through), fetal monitors, plumbing, circuit boards, jet engines, and ceramic glazes. In addition, lead miners and smelters, plumbers and fitters, auto mechanics, glass manufacturers, construction workers, battery manufacturers and recyclers, firing range instructors, and plastic manufacturers are at risk for lead exposure. Other occupations that present lead exposure risks include welding, manufacture of rubber, printing, zinc and copper smelting, processing of ore, combustion of solid waste, and production of paints and pigments. Parents who are exposed to lead in the workplace can bring lead dust home on clothes or skin and expose their children. Some lead compounds are colorful and are used widely in paints, and lead paint is a major route of lead exposure in children. It has been found that 38 million housing units in the US had lead-based paint, down from the 1990 estimate of 64 million. Deteriorating lead paint can produce dangerous lead levels in household dust and soil. Deteriorating lead paint and lead-containing household dust are the main causes of chronic lead poisoning. The lead breaks down into the dust and since children are more prone to crawling on the floor, it is easily ingested. Many young children display pica, eating things that are not food. Even a small amount of a lead-containing product such as a paint chip or a sip of glaze can contain tens or hundreds of milligrams of lead. Eating chips of lead paint presents a particular hazard to children, generally producing more severe poisoning than occurs from dust. Because removing lead paint from dwellings, e.g. by sanding or torching creates lead-containing dust and fumes, it is generally safer to seal the lead paint under new paint (excepting moveable windows and doors, which create paint dust when operated). Alternately, special precautions must be taken if the lead paint is to be removed. Residual lead in soil contributes to lead exposure in urban areas. It has been thought that the more polluted an area is with various contaminants, the more likely it is to contain lead. However, this is not always the case, as there are several other reasons for lead contamination in soil. Lead content in soil may be caused by broken-down lead paint, residues from lead-containing gasoline, used engine oil, or pesticides used in the past, contaminated landfills, or from nearby industries such as foundries or smelters. Although leaded soil is less of a problem in countries that no longer have leaded gasoline, it remains prevalent, raising concerns about the safety of urban agriculture; eating food grown in contaminated soil can present a lead hazard. Lead from the atmosphere or soil can end up in groundwater and surface water. It is also potentially in drinking water, e.g. from plumbing and fixtures that are either made of lead or have lead solder. Since acidic water breaks down lead in plumbing more readily, chemicals can be added to municipal water to increase the pH and thus reduce the corrosivity of the public water supply. Chloramines, which were adopted as a substitute for chlorine disinfectants due to fewer health concerns, increase corrositivity. In the US, 14–20% of total lead exposure is attributed to drinking water. In 2004, a team of seven reporters from The Washington Post discovered high levels of lead in the drinking water in Washington, D.C. and won an award for investigative reporting for a series of articles about this contamination. In Australia, collecting rainwater from roof runoff used as potable water may contain lead if there are lead contaminants on the roof or in the storage tank. The Australian Drinking Water Guidelines allow a maximum of .01 mg/L lead in water. Lead can be found in products such as kohl, an ancient cosmetic from the Middle East, South Asia, and parts of Africa that has many names; and from some toys. In 2007, millions of toys made in China were recalled from multiple countries owing to safety hazards including lead paint. Vinyl mini-blinds, found especially in older housing, may contain lead. Lead is commonly incorporated into herbal remedies such as Indian Ayurvedic preparations and remedies of Chinese origin. There are also risks of elevated blood lead levels caused by folk remedies like azarcon and greta, which each contain about 95% lead. Ingestion of metallic lead, such as small lead fishing lures, increases blood lead levels and can be fatal. Ingestion of lead-contaminated food is also a threat. Ceramic glaze often contains lead, and dishes that have been improperly fired can leach the metal into food, potentially causing severe poisoning. In some places, the solder in cans used for food contains lead. When manufacturing medical instruments and hardware, solder containing lead may be present. People who eat animals hunted with lead bullets may be at risk for lead exposure. Bullets lodged in the body rarely cause significant levels of lead poisoning, but bullets lodged in the joints are the exception, as they deteriorate and release lead into the body over time. Because game animals can be shot using lead bullets, the potential for consumption of game meat to represent an avenue for lead ingestion has seen clinical and epidemiological study. In a recent study conducted by the CDC, a cohort from North Dakota was enrolled and asked to self-report historical consumption of game meat, and participation in other activities that could cause lead exposure. The study found that participants' age, sex, housing age, current hobbies with potential for lead exposure, and game consumption were all associated with blood lead level (PbB). This study has been cited by popular media as simple evidence that hunting increases exposure to lead poisoning, prompting the University of Illinois Extension to release a statement that there is no such risk. Concerning the CDC report, the authors' conclusion in a related Epi-AID Trip Report notes the small increase associated with game consumption in the study, and urges interpretation with respect to environmental context: Some hunters][ may argue that lead-based bullets offer greater accuracy and more humane kills of game animals than might copper-based bullets, which represent the most commonly available, though expensive, alternative to lead. Bullet designs vary greatly, and some lead-based bullets are highly resistant to fragmentation, offering hunters the ability to clean game animals with negligible risk of including lead fragments in prepared meat. Other bullets are prone to fragmentation and exacerbate the risk of lead ingestion from prepared meat. In practice, use of a non-fragmenting bullet, and proper cleaning of the game animal's wound, can eliminate the risk of lead ingestion from eating game; however, isolating such practice to experimentally determine its association with blood lead levels in study is difficult to do. Bismuth is an element currently being introduced as a lead-replacement for shotgun pellets used in waterfowl hunting. The primary purpose is to prevent water contamination, however rather than making meat safe to consume.][ Lead birdshot is banned in some areas, but this is primarily for the benefit of wildfowl and their predators, rather than humans. Non-lead alternatives include steel, tungsten-nickel-iron, bismuth-tin, and tungsten-polymer. Exposure occurs through inhalation, ingestion or occasionally skin contact. Lead may be taken in through direct contact with mouth, nose, and eyes (mucous membranes), and through breaks in the skin. Tetraethyllead, which was a gasoline additive and is still used in fuels such as aviation fuel, passes through the skin; however inorganic lead found in paint, food, and most lead-containing consumer products is only minimally absorbed through the skin. The main sources of absorption of inorganic lead are from ingestion and inhalation. In adults, about 35–40% of inhaled lead dust is deposited in the lungs, and about 95% of that goes into the bloodstream. Of ingested inorganic lead, about 15% is absorbed, but this percentage is higher in children, pregnant women, and people with deficiencies of calcium, zinc, or iron. Children and infants may absorb about 50% of ingested lead, but little is known about absorption rates in children. The main body compartments that store lead are the blood, soft tissues, and bone; the half-life of lead in these tissues is measured in weeks for blood, months for soft tissues, and years for bone. Lead in the bones, teeth, hair, and nails is bound tightly and not available to other tissues, and is generally thought not to be harmful. In adults, 94% of absorbed lead is deposited in the bones and teeth, but children only store 70% in this manner, a fact which may partially account for the more serious health effects on children. The estimated half-life of lead in bone is 20 to 30 years, and bone can introduce lead into the bloodstream long after the initial exposure is gone. The half-life of lead in the blood in men is about 40 days, but it may be longer in children and pregnant women, whose bones are undergoing remodeling, which allows the lead to be continuously re-introduced into the bloodstream. Also, if lead exposure takes place over years, clearance is much slower, partly due to the re-release of lead from bone. Many other tissues store lead, but those with the highest concentrations (other than blood, bone, and teeth) are the brain, spleen, kidneys, liver, and lungs. It is removed from the body very slowly, mainly through urine. Smaller amounts of lead are also eliminated through the feces, and very small amounts in hair, nails, and sweat. Lead has no known physiologically relevant role in the body, and its harmful effects are myriad. Lead and other heavy metals create reactive radicals which damage cell structures including DNA and cell membranes. Lead also interferes with DNA transcription, enzymes that help in the synthesis of vitamin D, and enzymes that maintain the integrity of the cell membrane. Anemia may result when the cell membranes of red blood cells become more fragile as the result of damage to their membranes. Lead interferes with metabolism of bones and teeth and alters the permeability of blood vessels and collagen synthesis. Lead may also be harmful to the developing immune system, causing production of excessive inflammatory proteins; this mechanism may mean that lead exposure is a risk factor for asthma in children. 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. The primary cause of lead's toxicity is its interference with a variety of enzymes because it binds to sulfhydryl groups found on many enzymes. Part of lead's toxicity results from its ability to mimic other metals that take part in biological processes, which act as cofactors in many enzymatic reactions, displacing them at the enzymes on which they act. 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 or reactions. Among the essential metals with which lead interacts are calcium, iron, and zinc. One of the main causes for the pathology of lead is that it interferes with the activity of an essential enzyme called delta-aminolevulinic acid dehydratase, or ALAD, which is important in the biosynthesis of heme, the cofactor found in hemoglobin. Lead also inhibits the enzyme ferrochelatase, another enzyme involved in the formation of heme. Ferrochelatase catalyzes the joining of protoporphyrin and 2+Fe to form heme. Lead's interference with heme synthesis results in production of zinc protoporphyrin and the development of anemia. Another effect of lead's interference with heme synthesis is the buildup of heme precursors, such as aminolevulinic acid, which may be directly or indirectly harmful to neurons. Lead interferes with the release of neurotransmitters, chemicals used by neurons to send signals to other cells. It interferes with the release of glutamate, a neurotransmitter important in many functions including learning, by blocking NMDA receptors. The targeting of NMDA receptors is thought to be one of the main causes for lead's toxicity to neurons. A Johns Hopkins report found that in addition to inhibiting the NMDA receptor, lead exposure decreased the amount of the gene for the receptor in part of the brain. In addition, lead has been found in animal studies to cause programmed cell death in brain cells. Lead affects every one of the body's organ systems, especially the nervous system, but also the bones and teeth, the kidneys, and the cardiovascular, immune, and reproductive systems. Hearing loss and tooth decay have been linked to lead exposure, as have cataracts. Intrauterine and neonatal lead exposure promote tooth decay. Aside from the developmental effects unique to young children, the health effects experienced by adults are similar to those in children, although the thresholds are generally higher. Kidney damage occurs with exposure to high levels of lead, and evidence suggests that lower levels can damage kidneys as well. The toxic effect of lead causes nephropathy and may cause Fanconi syndrome, in which the proximal tubular function of the kidney is impaired. 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. Lead poisoning inhibits excretion of the waste product urate and causes a predisposition for gout, in which urate builds up. This condition is known as saturnine gout. Evidence suggests lead exposure is associated with high blood pressure, and studies have also found connections between lead exposure and coronary heart disease, heart rate variability, and death from stroke, but this evidence is more limited. 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. Lead affects both the male and female reproductive systems. In men, when blood lead levels exceed 40 μg/dL, sperm count is reduced and changes occur in volume of sperm, their motility, and their morphology. A pregnant woman's elevated blood lead level can lead to miscarriage, prematurity, low birth weight, and problems with development during childhood. Lead is able to pass through the placenta and into breast milk, and blood lead levels in mothers and infants are usually similar. 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; increased calcium intake in pregnancy may help mitigate this phenomenon. Lead affects the peripheral nervous system (especially motor nerves) and the central nervous system. Peripheral nervous system effects are more prominent in adults and central nervous system effects are more prominent in children. Lead causes the axons of nerve cells to degenerate and lose their myelin coats. The brain is the organ most sensitive to lead exposure. Lead is able to pass through the endothelial cells at the blood brain barrier because it can substitute for calcium ions and be uptaken by Calcium-ATPase pumps. 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. In a child's developing brain, lead interferes with synapse formation in the cerebral cortex, neurochemical development (including that of neurotransmitters), and organization of ion channels. It causes loss of neurons' myelin sheaths, reduces numbers of neurons, interferes with neurotransmission, and decreases neuronal growth. Lead exposure in young children has been linked to learning disabilities, and children with blood lead concentrations greater than 10 μg/dL are in danger of developmental disabilities. Increased blood lead level in children has been correlated with decreases in intelligence, nonverbal reasoning, short-term memory, attention, reading and arithmetic ability, fine motor skills, emotional regulation, and social engagement. The effect of lead on children's cognitive abilities takes place at very low levels. There is apparently no lower threshold to the dose-response relationship (unlike other heavy metals such as mercury). Reduced academic performance has been associated with lead exposure even at blood lead levels lower than 5 μg/dL. Blood lead levels below 10 μg/dL have been reported to be associated with lower IQ and behavior problems such as aggression, in proportion with blood lead levels. Between the blood lead levels of 5 and 35 μg/dL, an IQ decrease of 2–4 points for each μg/dL increase is reported in children. High blood lead levels in adults are also associated with decreases in cognitive performance and with psychiatric symptoms such as depression and anxiety. 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. Increases in blood lead levels from about 50 to about 100 μg/dL in adults have been found to be associated with persistent, and possibly permanent, impairment of central nervous system function. Lead exposure in children is also correlated with neuropsychiatric disorders such as attention deficit hyperactivity disorder and antisocial behavior. Elevated lead levels in children are correlated with higher scores on aggression and delinquency measures. A correlation has also been found between prenatal and early childhood lead exposure and violent crime in adulthood. Countries with the highest air lead levels have also been found to have the highest murder rates, after adjusting for confounding factors. 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 US. A 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 countries. It is believed that the U.S. ban on lead paint in buildings in the late 1970s, as well as the phaseout of leaded gasoline in the 1970s and 1980s, partially helped contribute to the decline of violent crime in the United States since the early 1990s. Diagnosis includes determining the clinical signs and the medical history, with inquiry into possible routes of exposure. Clinical toxicologists, medical specialists in the area of poisoning, may be involved in diagnosis and treatment. The main tool in diagnosing and assessing the severity of lead poisoning is laboratory analysis of the blood lead level (BLL). Blood film examination may reveal basophilic stippling of red blood cells (dots in red blood cells visible through a microscope), as well as the changes normally associated with iron-deficiency anemia (microcytosis and hypochromasia). However, basophilic stippling is also seen in unrelated conditions, such as megaloblastic anemia caused by vitamin B12 (colbalamin) and folate deficiencies. 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, with a delay of a few weeks. Thus EP levels in conjunction with blood lead levels can suggest the time period of exposure; if blood lead levels are high but EP is still normal, this finding suggests exposure was recent. However, the EP level alone is not sensitive enough to identify elevated blood lead levels below about 35 μg/dL. Due to this higher threshold for detection and the fact that EP levels also increase in iron deficiency, use of this method for detecting lead exposure has decreased. Blood lead levels are an indicator mainly of recent or current lead exposure, not of total body burden. Lead in bones can be measured noninvasively by X-ray fluorescence; this may be the best measure of cumulative exposure and total body burden. However this method is not widely available and is mainly used for research rather than routine diagnosis. 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, especially around the knees. These lead lines, caused by increased calcification due to disrupted metabolism in the growing bones, 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. 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. 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. Lead poisoning shares symptoms with other conditions and may be easily missed. Conditions that present similarly and must be ruled out in diagnosing lead poisoning include carpal tunnel syndrome, Guillain-Barré syndrome, renal colic, appendicitis, encephalitis in adults, and viral gastroenteritis in children. Other differential diagnoses in children include constipation, abdominal colic, iron deficiency, subdural hematoma, neoplasms of the central nervous system, emotional and behavior disorders, and mental retardation. The current reference range for acceptable blood lead concentrations in healthy persons without excessive exposure to environmental sources of lead is less than 5 µg/dL for children. It was less than 25 µg/dL for adults. Previous to 2012 the value for children was 10 (µg/dl). The current biological exposure index (a level that should not be exceeded) for lead-exposed workers in the U.S. is 30 µg/dL in a random blood specimen. The National Institute for Occupational Safety and Health (CDC/NIOSH) reference blood lead level in adults is 10 μg/dL The U.S. national BLL geometric mean among adults was 1.2 μg/dL in 2009–2010 Blood lead concentrations in poisoning victims have ranged from 30->80 µg/dL in children exposed to lead paint in older houses, 77–104 µg/dL in persons working with pottery glazes, 90–137 µg/dL in individuals consuming contaminated herbal medicines, 109–139 µg/dL in indoor shooting range instructors and as high as 330 µg/dL in those drinking fruit juices from glazed earthenware containers. In most cases, lead poisoning is preventable by avoiding exposure to lead. Prevention strategies can be divided into individual (measures taken by a family), preventive medicine (identifying and intervening with high-risk individuals), and public health (reducing risk on a population level). 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, discouraging them from putting their hands to their mouths, vacuuming frequently, and eliminating the presence of lead-containing objects such as blinds and jewellery in the house. In houses with lead pipes or plumbing solder, these can be replaced. Less permanent but cheaper methods include running water in the morning to flush out the most contaminated water, or adjusting the water's chemistry to prevent corrosion of pipes. Lead testing kits are commercially available for detecting the presence of lead in the household. Also use only cold water from the tap for drinking, cooking, and for making baby formula. Hot water is more likely than cold water to contain higher amounts of lead. Since most of the lead in household water usually comes from plumbing in the house and not from the local water supply, using cold water can avoid lead exposure. Screening is an important method in preventive medicine strategies. Screening programs exist to test the blood of children at high risk for lead exposure, such as those who live near lead-related industries. Prevention measures also exist on national and municipal levels. 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, water, air, household dust, and products. Regulations exist to limit the amount of lead in paint; for example, a 1978 law in the US restricted the lead in paint for residences, furniture, and toys to 0.06% or less. In October 2008, the US Environmental Protection Agency reduced the allowable lead level by a factor of ten to 0.15 micrograms per cubic meter of air, giving states five years to comply with the standards. The European Union's Restriction of Hazardous Substances Directive limits amounts of lead and other toxic substances in electronics and electrical equipment. In some places, remediation programs exist to reduce the presence of lead when it is found to be high, for example in drinking water. As a more radical solution, entire towns located near former lead mines have been "closed" by the government, and the population resettled elsewhere, as was the case with Picher, Oklahoma in 2009. The mainstays of treatment are removal from the source of lead and, for people who have significantly high blood lead levels or who have symptoms of poisoning, chelation therapy. Treatment of iron, calcium, and zinc deficiencies, which are associated with increased lead absorption, is another part of treatment for lead poisoning. When lead-containing materials are present in the gastrointestinal tract (as evidenced by abdominal X-rays), whole bowel irrigation, cathartics, endoscopy, or even surgical removal may be used to eliminate it from the gut and prevent further exposure. 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 or synovial spaces. If lead encephalopathy is present, anticonvulsants may be given to control seizures, and treatments to control swelling of the brain include corticosteroids and mannitol. Treatment of organic lead poisoning involves removing the lead compound from the skin, preventing further exposure, treating seizures, and possibly chelation therapy for people with high blood lead concentrations. 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, such as lead. The chelate that is thus formed is nontoxic and can be excreted in the urine, initially at up to 50 times the normal rate. The chelating agents used for treatment of lead poisoning are edetate disodium calcium (EDTA2CaNa), dimercaprol (BAL), which are injected, and succimer and d-penicillamine, which are administered orally. Chelation therapy is used in cases of acute lead poisoning, severe poisoning, and encephalopathy, and is considered for people with blood lead levels above 25 µg/dL. While the use of chelation for people with symptoms of lead poisoning is widely supported, 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. Chelation therapy is usually stopped when symptoms resolve or when blood lead levels return to premorbid levels. When lead exposure has taken place over a long period, blood lead levels may rise after chelation is stopped because lead is leached into blood from stores in the bone; thus repeated treatments are often necessary. People receiving dimercaprol need to be assessed for peanut allergies since the commercial formulation contains peanut oil. Calcium EDTA is also effective if administered four hours after the administration of dimercaprol. Administering dimercaprol prior to calcium EDTA is necessary to prevent the redistribution of lead into the central nervous system. An adverse side effect of calcium EDTA is renal toxicity. Succimer is the preferred agent in mild lead poisoning cases. This may be the case in instances where children have a blood lead level >25μg/dL. The most reported adverse side effect for succimer is gastrointestinal disturbances. It is also important to note that chelation therapy only lowers blood lead levels and may not prevent the lead-induced cognitive problems associated with lower lead levels in tissue. This may be because of the inability of these agents to remove sufficient amounts of lead from tissue or inability to reverse preexisting damage. Chelating agents can have adverse effects; for example, chelation therapy can lower the body's levels of necessary nutrients like zinc. Chelating agents taken orally can increase the body's absorption of lead through the intestine. Chelation challenge, also known as provocation testing, is used to indicate an elevated and mobilizable body burden of heavy metals including lead. This testing involves collecting urine before and after administering a one-off dose of chelating agent to mobilize heavy metals into the urine. Then urine is analyzed by a laboratory for levels of heavy metals; from this analysis overall body burden is inferred. Chelation challenge mainly measures the burden of lead in soft tissues, and may not accurately reflect long-term exposure or the amount of lead stored in bone. Although the technique has been used to determine whether chelation therapy is indicated and to diagnose heavy metal exposure, evidence does not support either of these uses as blood levels after chelation are not comparable to the reference range typically used to diagnose heavy metal poisoning. The single chelation dose could also redistribute the heavy metals to more sensitive areas such as central nervous system tissue. Since lead has been used widely for centuries, the effects of exposure are worldwide. Environmental lead is ubiquitous, and everyone has some measurable blood lead level. Lead is one of the largest environmental medicine problems in terms of numbers of people exposed and the public health toll it takes. Lead exposure accounts for about 0.2% of all deaths and 0.6% of disability adjusted life years globally. Although regulation reducing lead in products has greatly reduced exposure in the developed world since the 1970s, lead is still allowed in products in many developing countries. In all countries that have banned leaded gasoline, average blood lead levels have fallen sharply. However, some developing countries still allow leaded gasoline, which is the primary source of lead exposure in most developing countries. Beyond exposure from gasoline, the frequent use of pesticides in developing countries adds a risk of lead exposure and subsequent poisoning. Poor children in developing countries are at especially high risk for lead poisoning. Of North American children, 7% have blood lead levels above 10 μg/dL, whereas among Central and South American children, the percentage is 33 to 34%. About one fifth of the world's disease burden from lead poisoning occurs in the Western Pacific, and another fifth is in Southeast Asia. In developed countries, nonwhite people with low levels of education living in poorer areas are most at risk for elevated lead. In the US, the groups most at risk for lead exposure are the impoverished, city-dwellers, and immigrants. African-American children and those living in old housing have also been found to be at elevated risk for high blood lead levels in the US. Low-income people often live in old housing with lead paint, which may begin to peel, exposing residents to high levels of lead-containing dust. Risk factors for elevated lead exposure include alcohol consumption and smoking (possibly because of contamination of tobacco leaves with lead-containing pesticides). Adults with certain risk factors might be more susceptible to toxicity; these include calcium and iron deficiencies, old age, disease of organs targeted by lead (e.g. the brain, the kidneys), and possibly genetic susceptibility. Differences in vulnerability to lead-induced neurological damage between males and females have also been found, but some studies have found males to be at greater risk, while others have found females to be. In adults, blood lead levels steadily increase with increasing age. In adults of all ages, men have higher blood lead levels than women do. Children are more sensitive to elevated blood lead levels than adults are. Children may also have a higher intake of lead than adults; they breathe faster and may be more likely to have contact with and ingest soil. Children ages one to three tend to have the highest blood lead levels, possibly because at that age they begin to walk and explore their environment, and they use their mouths in their exploration. Blood levels usually peak at about 18–24 months old. In many countries including the US, household paint and dust are the major route of exposure in children. Outcome is related to the extent and duration of lead exposure. Effects of lead on the physiology of the kidneys and blood are generally reversible; its effects on the central nervous system are not. While peripheral effects in adults often go away when lead exposure ceases, evidence suggests that most of lead's effects on a child's central nervous system are irreversible. Children with lead poisoning may thus have adverse health, cognitive, and behavioral effects that follow them into adulthood. Lead encephalopathy is a medical emergency and causes permanent brain damage in 70–80% of children affected by it, even those that receive the best treatment. The mortality rate for people who develop cerebral involvement is about 25%, and of those who survive who had lead encephalopathy symptoms by the time chelation therapy was begun, about 40% have permanent neurological problems such as cerebral palsy. Exposure to lead may also decrease lifespan and have health effects in the long term. Death rates from a variety of causes have been found to be higher in people with elevated blood lead levels; these include cancer, stroke, and heart disease, and general death rates from all causes. Lead is considered a possible human carcinogen based on evidence from animal studies. Evidence also suggests that age-related mental decline and psychiatric symptoms are correlated with lead exposure. Cumulative exposure over a prolonged period may have a more important effect on some aspects of health than recent exposure. Some health effects, such as high blood pressure, are only significant risks when lead exposure is prolonged (over about one year). Lead poisoning was among the first known and most widely studied work and environmental hazards. One of the first metals to be smelted and used, lead is thought to have been discovered and first mined in Anatolia around 6500 BC. Its density, workability, and corrosion-resistance were among the metal's attractions. In the 2nd century BC the Greek botanist Nicander described the colic and paralysis seen in lead-poisoned people. Dioscorides, a Greek physician who lived in the 1st century CE, wrote that lead makes the mind "give way". Lead was used extensively in Roman aqueducts from about 500 BC to 300 AD Julius Caesar's engineer, Vitruvius, 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 is produced by it, and this is said to be harmful to the human body." Gout, prevalent in affluent Rome, is thought to be the result of lead, or leaded eating and drinking vessels. Sugar of lead (Lead II Acetate) was used to sweeten wine, and the gout that resulted from this was known as "saturnine" gout. It is even hypothesized that lead poisoning may have contributed to the decline of the Roman Empire, a hypothesis thoroughly disputed: It has been noted that Romans also consumed quantities of lead through the consumption of defrutum, carenum, and sapa, musts made by boiling down fruit in lead cookware. Defrutum and its relatives were used in Ancient Roman cuisine and cosmetics, including as a food preservative. However, the use of leaden cookware, though popular, was not the general standard and copper cookware was used far more generally. Additionally there is also no indication how often sapa was added or in what quantity. The consumption of sapa as having a role in the fall of the Roman Empire was used in a theory proposed by geochemist Jerome Nriagu to state that "lead poisoning contributed to the decline of the Roman Empire". John Scarborough, a pharmacologist and classicist, criticized the conclusions drawn by Nriagu's book as "so full of false evidence, miscitations, typographical errors, and a blatant flippancy regarding primary sources that the reader cannot trust the basic arguments." After antiquity, mention of lead poisoning was absent from medical literature until the end of the Middle Ages. In 1656 the German physician Samuel Stockhausen recognized dust and fumes containing lead compounds as the cause of disease, called since ancient Roman times morbi metallici, that were known to afflict miners, smelter workers, potters, and others whose work exposed them to the metal. The painter Caravaggio might have died of lead poisoning. Bones with high lead levels were recently found in a grave thought likely to be Caravaggio's grave. Paints used at the time contained high amounts of lead salts. Caravaggio is known to have indulged in violent behavior, as caused by lead poisoning. In 17th-century Germany, the physician Eberhard Gockel discovered lead-contaminated wine to be the cause of an epidemic of colic. He had noticed that monks who did not drink wine were healthy, while wine drinkers developed colic, and traced the cause to sugar of lead, made by simmering litharge with vinegar. As a result, Eberhard Ludwig, Duke of Württemberg issued an edict in 1696 banning the adulteration of wines with litharge. In the 18th century lead poisoning was fairly frequent on account of the widespread drinking of rum, which was made in stills with a lead component (the "worm"). It was a significant cause of mortality amongst slaves and sailors in the colonial West Indies. Lead poisoning from rum was also noted in Boston. The famous Benjamin Franklin suspected lead to be a risk in 1786. Also in the 18th century, "Devonshire colic" was the name given to the symptoms suffered by people of Devon who drank cider made in presses that were lined with lead. Lead was added to cheap wine illegally in the 18th and early 19th centuries as a sweetener. The composer Beethoven, a heavy wine drinker, suffered elevated lead levels (as later detected in his hair) possibly due to this; the cause of his death is controversial, but lead poisoning is a contender as a factor. With the Industrial Revolution in the 19th century, lead poisoning became common in the work setting. The introduction of lead paint for residential use in the 19th century increased childhood exposure to lead; for millennia before this, most lead exposure had been occupational. An important step in the understanding of childhood lead poisoning occurred when toxicity in children from lead paint was recognized in Australia in 1897. France, Belgium, and Austria banned white lead interior paints in 1909; the League of Nations followed suit in 1922. However, in the United States, laws banning lead house paint were not passed until 1971, and it was phased out and not fully banned until 1978. The 20th century saw an increase in worldwide lead exposure levels due to the increased widespread use of the metal. Beginning in the 1920s, lead was added to gasoline to improve its combustion; lead from this exhaust persists today in soil and dust in buildings. Blood lead levels worldwide have been declining sharply since the 1980s, when leaded gasoline began to be phased out. In those countries that have banned lead in solder for food and drink cans and have banned leaded gasoline additives, blood lead levels have fallen sharply since the mid-1980s. The levels found today in most people are orders of magnitude greater than those of pre-industrial society. Due to reductions of lead in products and the workplace, acute lead poisoning is rare in most countries today; however, low level lead exposure is still common. It was not until the second half of the 20th century that subclinical lead exposure became understood to be a problem. During the end of the 20th century, the blood lead levels deemed acceptable steadily declined. Blood lead levels once considered safe are now considered hazardous, with no known safe threshold. 15,000 people are being relocated from Jiyuan in central Henan province to other locations after 1000 children living around China's largest smelter plant (owned and operated by Yuguang Gold and Lead) were found to have excess lead in their blood. The total cost of this project is estimated to around 1 billion yuan ($150 million). 70% of the cost will be paid by local government and the smelter company, while the rest will be paid by the residents themselves. The government has suspended production at 32 of 35 lead plants. The affected area includes people from 10 different villages. The Zamfara State lead poisoning epidemic occurred in Nigeria in 2010. As of October 5, 2010 at least 400 children have died from the effects of lead poisoning. Humans are not alone in suffering from lead's effects; plants and animals are also affected by lead toxicity to varying degrees depending on species. Animals experience many of the same effects of lead exposure as humans do, such as abdominal pain, peripheral neuropathy, and behavioral changes such as increased aggression. Much of what is known about human lead toxicity and its effects is derived from animal studies. Animals are used to test the effects of treatments, such as chelating agents, and to provide information on the pathophysiology of lead, such as how it is absorbed and distributed in the body. Farm animals such as cows and horses as well as pet animals are also susceptible to the effects of lead toxicity. Sources of lead exposure in pets can be the same as those that present health threats to humans sharing the environment, such as paint and blinds, and there is sometimes lead in toys made for pets. Lead poisoning in a pet dog may indicate that children in the same household are at increased risk for elevated lead levels. Lead, one of the leading causes of toxicity in waterfowl, has been known to cause die-offs of wild bird populations. When hunters use lead shot, waterfowl such as ducks can ingest the spent pellets later and be poisoned; predators that eat these birds are also at risk. Lead shot-related waterfowl poisonings 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 waterfowl deaths. Lead shot has been banned for hunting waterfowl in several countries, including the US in 1991 and 1997 in Canada. Other threats to wildlife include lead paint, sediment from lead mines and smelters, and lead weights from fishing lines. Lead in some fishing gear has been banned in several countries. The critically endangered California Condor has also been affected by lead poisoning. As scavengers, condors eat carcasses of game that have been shot but not retrieved, and with them the fragments from lead bullets; this increases their lead levels. Among condors around the Grand Canyon, lead poisoning due to eating lead shot is the most frequently diagnosed cause of death. In an effort to protect this species, in areas designated as the California Condor's range the use of projectiles containing lead has been banned to hunt deer, feral pigs, elk, pronghorn antelope, coyotes, ground squirrels, and other non-game wildlife. Also, conservation programs exist which routinely capture condors, check their blood lead levels, and treat cases of poisoning.
M: TOX gen / txn pto ant vitiligo: Quadrichrome vitiligo  Vitiligo ponctué  syndromic (Alezzandrini syndrome  Vogt–Koyanagi–Harada syndrome)
albinism: Oculocutaneous albinism  Ocular albinism melanosome transfer: Hermansky–Pudlak syndrome  Chédiak–Higashi syndrome  Griscelli syndrome (Elejalde syndrome  Griscelli syndrome type 2  Griscelli syndrome type 3) Lentigo/Lentiginosis: Lentigo simplex  Liver spot  Centrofacial lentiginosis  Generalized lentiginosis  Inherited patterned lentiginosis in black persons  Ink spot lentigo  Lentigo maligna  Mucosal lentigines  Partial unilateral lentiginosis  PUVA lentigines M: INT, SF, LCT anat/phys/devp noco (i/b/d/q/u/r/p/m/k/v/f)/cong/tumr (n/e/d), sysi/epon proc, drug (D2/3/4/5/8/11)
In the context of biology, poisons are substances that cause disturbances to organisms, usually by chemical reaction or other activity on the molecular scale, when a sufficient quantity is absorbed by an organism. The fields of medicine (particularly veterinary) and zoology often distinguish a poison from a toxin, and from a venom. Toxins are poisons produced by some biological function in nature, and venoms are usually defined as toxins that are injected by a bite or sting to cause their effect, while other poisons are generally defined as substances absorbed through epithelial linings such as the skin or gut. Some poisons are also toxins, usually referring to naturally produced substances, such as the bacterial proteins that cause tetanus and botulism. A distinction between the two terms is not always observed, even among scientists. Animal poisons that are delivered subcutaneously (e.g. by sting or bite) are also called venom. In normal usage, a poisonous organism is one that is harmful to consume, but a venomous organism uses poison (venom) to kill its prey or defend itself while still alive. A single organism can be both poisonous and venomous. The derivative forms "toxic" and "poisonous" are synonymous. In nuclear physics, a poison is a substance that obstructs or inhibits a nuclear reaction. For an example, see nuclear poison. The term "poison" is often used colloquially to describe any harmful substance, particularly corrosive substances, carcinogens, mutagens, teratogens and harmful pollutants, and to exaggerate the dangers of chemicals. Paracelsus, the father of toxicology, once wrote: "Everything is poison, there is poison in everything. Only the dose makes a thing not a poison." (see Median lethal dose) The legal definition of "poison" is stricter. A medical condition of poisoning can also be caused by substances that are not legally required to carry the label "poison". Environmentally hazardous substances are not necessarily poisons and vice versa. For example, food industry wastewater—which may contain potato juice or milk—can be hazardous to the ecosystems of streams and rivers by consuming oxygen and causing eutrophication, but is nonhazardous to humans and not classified as a poison. The term poison with regard to biology and chemistry is often misused due to lack of a universal definition. Biologically speaking, any substance, if given in large enough amounts, is poisonous and can cause death. For instance, while botulinum toxin is lethal on the level of nanograms, a person would have to ingest kilograms worth of water to receive a lethal dose. While there may be a large disparity in this example, there are many substances used as medications where the LD50 is only one order of magnitude greater than the ED50 such as fentanyl. A better definition would distinguish between lethal substances that provide a therapeutic value and those that do not. The lack of a mathematical definition for the term poison impedes a universal definition. Acute poisoning is exposure to a poison on one occasion or during a short period of time. Symptoms develop in close relation to the exposure. Absorption of a poison is necessary for systemic poisoning. In contrast, substances that destroy tissue but do not absorb, such as lye, are classified as corrosives rather than poisons. Furthermore, many common household medications are not labeled with skull and crossbones, although they can cause severe illness or even death. In the medical sense, poisoning can be caused by less dangerous substances than those receiving the legal classification of "poison". Chronic poisoning is long-term repeated or continuous exposure to a poison where symptoms do not occur immediately or after each exposure. The patient gradually becomes ill, or becomes ill after a long latent period. Chronic poisoning most commonly occurs following exposure to poisons that bioaccumulate, or are biomagnified, such as mercury and lead. Contact or absorption of poisons can cause rapid death or impairment. Agents that act on the nervous system can paralyze in seconds or less, and include both biologically derived neurotoxins and so-called nerve gases, which may be synthesized for warfare or industry. Inhaled or ingested cyanide, used as a method of execution in gas chambers, almost instantly starves the body of energy by inhibiting the enzymes in mitochondria that make ATP. Intravenous injection of an unnaturally high concentration of potassium chloride, such as in the execution of prisoners in parts of the United States, quickly stops the heart by eliminating the cell potential necessary for muscle contraction. Most biocides, including pesticides, are created to act as poisons to target organisms, although acute or less observable chronic poisoning can also occur in non-target organism, including the humans who apply the biocides and other beneficial organisms. For example, the herbicide 2,4-D imitates the action of a plant hormone, to the effect that the lethal toxicity is specific to plants. Indeed, 2,4-D is not a poison, but classified as "harmful" (EU). Many substances regarded as poisons are toxic only indirectly, by toxication. An example is "wood alcohol" or methanol, which is not poisonous itself, but is chemically converted to toxic formaldehyde and formic acid in the liver. Many drug molecules are made toxic in the liver, and the genetic variability of certain liver enzymes makes the toxicity of many compounds differ between individuals. Toxicology is the study of the symptoms, mechanisms, treatment and diagnosis of biological poisoning. Exposure to radioactive substances can produce radiation poisoning, an unrelated phenomenon. Some poisons have specific antidotes: In 2010, poisoning resulted in about 180,000 deaths down from 200,000 in 1990. There were approximately 727,500 emergency department visits in the United States involving poisonings-- 3.3% of all injury-related encounters. Throughout human history, intentional application of poison has been used as a method of murder, pest-control,suicide, and execution. As a method of execution, poison has been ingested, as the ancient Athenians did (see Socrates), inhaled, as with carbon monoxide or hydrogen cyanide (see gas chamber), or injected (seelethal injection). Many languages describe lethal injection with their corresponding words for "poison shot"][. Poison's lethal effect can be combined with its allegedly magical powers; an example is the Chinese poisongu. Poison was also employed in gunpowder warfare. For example, the 14th-century Chinese text of the Huolongjing written by Jiao Yu outlined the use of a poisonous gunpowder mixture to fill cast iron grenade bombs. M: TOX gen / txn pto ant M: TOX gen / txn pto ant
meso-2,3-dimercaptosuccinic acid succimer, APRD01236 (Drugbank), Chemet O=C(O)[C@@H](S)[C@@H](S)C(=O)O InChI=1S/C4H6O4S2/c5-3(6)1(9)2(10)4(7)8/h1-2,9-10H,(H,5,6)(H,7,8)/t1-,2+ 
Key: ACTRVOBWPAIOHC-XIXRPRMCSA-N  InChI=1/C4H6O4S2/c5-3(6)1(9)2(10)4(7)8/h1-2,9-10H,(H,5,6)(H,7,8)/t1-,2+
Key: ACTRVOBWPAIOHC-XIXRPRMCBX 125 °C, 398 K, 257 °F Dimercaptosuccinic acid (DMSA), is the organosulfur compound with the formula HO2CCH(SH)CH(SH)CO2H. This colorless solid contains two carboxylic acid and two thiol groups, the latter being responsible for its mildly unpleasant odour. It occurs in two diastereomers, meso and the chiral dl forms. The meso isomer is used as a chelating agent. DMSA was first synthesized by V. Nirenburg in the Urals Polytechnic Institute, commissioned by one of the electrical enterprises of Sverdlovsk, which consumed many tons of mercury and was looking for a medicine to prevent poisoning of personnel. In 1957, it was found by Chinese scientists that DMSA can effectively treat antimony poisoning due to overdose of tartar emetic. Pronounced protective effect in animal poisoning with arsenic and mercury was first shown by I. Okonishnikova in 1962. The 2,3-dimercaptosuccinic acid molecule has two stereocentres (two asymmetric carbons), and can exist as three different stereoisomers. The 2S,3S and 2R,3R isomers are a pair of enantiomers, whereas the 2R,3S isomer is a meso compound and thus optically inactive. DMSA may be prepared by reacting acetylenedicarboxylic acid with sodium thiosulfate or thioacetic acid followed by hydrolysis. The dimethyl ester is also known. Meso 2,3-dimercaptosuccinic acid binds to "soft" heavy metals such as 2+Hg and 2+Pb, mobilizing these ions for excretion. It binds to metal cations through the thiol groups, which ionize upon complexation. Dimercaptosuccinic acid (CHEMET) is indicated for the treatment of lead poisoning in children with blood level measured above 45 µg/dL. The use of DMSA is not approved for prophylactic/prevention of lead poisoning in anticipation of exposure in known lead contaminated environments. Its elimination half-life is 2.5-3.5 h. DMSA can cross the blood–brain barrier of mice, but not that of humans, limiting its use to extracting heavy metals from parts of the body other than the central nervous system. Another application for DMSA is for provocation of tissue heavy metals in anticipation of a urine test. This is sometimes called a "challenge" or "provoked" heavy metals test. DMSA is used to help mobilize heavy metals stored in body tissues (and therefore not typically present in the circulation) and increase the excretion of heavy metals in the urine. In a study by Howard Frumkin et al., this sort of test was shown to not reliably provide an indication of past chronic mercury exposure, something it was often used for. A 2004 study by GP Archbold, et al. called the results of a DMSA challenge test "misleading" for the purposes of diagnosing mercury toxicity. Moreover, DMSA share the limitation of extracellular distribution, which makes it unable to cross the cell membrane and chelate heavy metals from intracellular sites. The relative activities of a series of novel monoalkyl esters of meso-2,3-dimercaptosuccinic acid (MiADMSA) have been examined as agents for the mobilization of cadmium, lead and arsenic owing to the ability of these monoesters to cross cell membranes. The monoesters were found to be more effective than the parent compound DMSA. The complexes (monoesters of DMSA) seem to penetrate cells (not possible in the case of DMSA), which helps in targeting intracellular sites in the body and aids in the removal of toxic metal ions in the cytosol and organelles inside the cell. M: TOX gen / txn pto ant
Mercury poisoning (also known as hydrargyria or mercurialism) is a disease caused by exposure to mercury or its compounds. Mercury (chemical symbol Hg) is a heavy metal occurring in several forms, all of which can produce toxic effects in high enough doses. Its zero oxidation state Hg0 exists as vapor or as liquid metal, its mercurous state Hg22+ exists as inorganic salts, and its mercuric state Hg2+ may form either inorganic salts or organomercury compounds; the three groups vary in effects. Toxic effects include damage to the brain, kidney, and lungs. Mercury poisoning can result in several diseases, including acrodynia (pink disease), Hunter-Russell syndrome, and Minamata disease. Symptoms typically include sensory impairment (vision, hearing, speech), disturbed sensation and a lack of coordination. The type and degree of symptoms exhibited depend upon the individual toxin, the dose, and the method and duration of exposure. Common symptoms of mercury poisoning include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), swelling, and desquamation (shedding of skin). Mercury irreversibly inhibits selenium-dependent enzymes (see below) and may also inactivate S-adenosyl-methionine, which is necessary for catecholamine catabolism by catechol-o-methyl transferase. Due to the body's inability to degrade catecholamines (e.g. epinephrine), a person suffering from mercury poisoning may experience profuse sweating, tachycardia (persistently faster-than-normal heart beat), increased salivation, and hypertension (high blood pressure). Affected children may show red cheeks, nose and lips, loss of hair, teeth, and nails, transient rashes, hypotonia (muscle weakness), and increased sensitivity to light. Other symptoms may include kidney dysfunction (e.g. Fanconi syndrome) or neuropsychiatric symptoms such as emotional lability, memory impairment, and / or insomnia. Thus, the clinical presentation may resemble pheochromocytoma or Kawasaki disease. An example of desquamation (skin peeling) of the hand of a child with severe mercury poisoning acquired by handling elemental mercury is this photograph in Horowitz, et al. (2002). The consumption of fish is by far the most significant source of ingestion-related mercury exposure in humans and animals, although plants and livestock also contain mercury due to bioconcentration of mercury from seawater, freshwater, marine and lacustrine sediments, soils, and atmosphere, and due to biomagnification by ingesting other mercury-containing organisms. Exposure to mercury can occur from breathing contaminated air, from eating foods that have acquired mercury residues during processing, from exposure to mercury vapor in mercury amalgam dental restorations, and from improper use or disposal of mercury and mercury-containing objects, for example, after spills of elemental mercury or improper disposal of fluorescent lamps. Consumption of whale and dolphin meat, as is the practice in Japan, is a source of high levels of mercury poisoning. Tetsuya Endo, a professor at the Health Sciences University of Hokkaido, has tested whale meat purchased in the whaling town of Taiji and found mercury levels more than 20 times the acceptable Japanese standard. Human-generated sources, such as coal-fired power plants, emit about half of atmospheric mercury, with natural sources such as volcanoes responsible for the remainder. An estimated two-thirds of human-generated mercury comes from stationary combustion, mostly of coal. Other important human-generated sources include gold production, nonferrous metal production, cement production, waste disposal, human crematoria, caustic soda production, pig iron and steel production, mercury production (mostly for batteries), and biomass burning. Small independent gold-mining operation workers are at higher risk of mercury poisoning because of crude processing methods. Such is the danger for the galamsey in Ghana and similar workers known as orpailleurs in neighboring francophone countries. While no official government estimates of the labor force have been made, observers believe 20,000-50,000 work as galamseys in Ghana, a figure including many women, who work as porters. Mercury and many of its chemical compounds, especially organomercury compounds, can also be readily absorbed through direct contact with bare, or in some cases (such as methylmercury) insufficiently protected, skin. Mercury and its compounds are commonly used in chemical laboratories, hospitals, dental clinics, and facilities involved in the production of items such as fluorescent light bulbs, batteries, and explosives. Mercury is highly reactive with selenium, an essential dietary element required by about 25 genetically distinct enzyme types (selenoenzymes). Among their numerous functions, selenoenzymes prevent and reverse oxidative damage in the brain and endocrine organs. The molecular mechanism of mercury toxicity involves its unique ability to irreversibly inhibit activities of selenoenzymes, such as thioredoxin reductase (IC50 = 9 nM). Although it has many additional functions, thioredoxin reductase restores vitamins C and E, as well as a number of other important antioxidant molecules, back into their reduced forms, enabling them to counteract oxidative damage within body cells. Since the rate of oxygen consumption is particularly high in brain tissues, production of reactive oxygen species (ROS) is accentuated in these vital cells, making them particularly vulnerable to oxidative damage and especially dependent upon the antioxidant protection provided by selenoenzymes. High mercury exposures deplete the amount of cellular selenium available for the biosynthesis of thioredoxin reductase and other selenoenzymes that prevent and reverse oxidative damage, which, if the depletion is severe and long lasting, results in brain cell dysfunctions that can ultimately cause death. High exposures to mercury in its various forms are particularly toxic to fetuses and infants. Women who have been exposed to mercury in substantial excess of dietary selenium intakes during pregnancy are at risk of giving birth to children with serious birth defects. Mercury exposures in excess of dietary selenium intakes in young children can have severe neurological consequences, preventing nerve sheaths from forming properly. Mercury inhibits the formation of myelin. According to some evidence, mercury poisoning may predispose to Young's syndrome (men with bronchiectasis and low sperm count). Because of differences in tissue distributions, mercury poisoning's effects will differ depending on whether it has been caused by exposure to elemental mercury, inorganic mercury compounds (as salts), or organomercury compounds. Quicksilver (liquid metallic mercury) is poorly absorbed by ingestion and skin contact. It is hazardous due to its potential to release mercury vapor. Animal data indicate less than 0.01% of ingested mercury is absorbed through the intact gastrointestinal tract, though it may not be true for individuals suffering from ileus. Cases of systemic toxicity from accidental swallowing are rare, and attempted suicide via intravenous injection does not appear to result in systemic toxicity. Though not studied quantitatively, 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, skin absorption would not be high. Some mercury vapor is absorbed dermally, but uptake by this route is only about 1% of that by inhalation. In humans, approximately 80% of inhaled mercury vapor is absorbed via the respiratory tract, where it enters the circulatory system and is distributed throughout the body. Chronic exposure by inhalation, even at low concentrations in the range 0.7–42 μg/m3, has been shown in case control studies to cause effects such as tremors, impaired cognitive skills, and sleep disturbance in workers. Acute inhalation of high concentrations causes a wide variety of cognitive, personality, sensory, and motor disturbances. The most prominent symptoms include tremors (initially affecting the hands and sometimes spreading to other parts of the body), emotional lability (characterized by irritability, excessive shyness, confidence loss, and nervousness), insomnia, memory loss, neuromuscular changes (weakness, muscle atrophy, muscle twitching), headaches, polyneuropathy (paresthesia, stocking-glove sensory loss, hyperactive tendon reflexes, slowed sensory and motor nerve conduction velocities), and performance deficits in tests of cognitive function. Mercury occurs inorganically as salts such as mercury(II) chloride. Mercury salts affect primarily the gastrointestinal tract and the kidneys, and can cause severe kidney damage; however, as they cannot cross the blood–brain barrier easily, mercury salts inflict little neurological damage without continuous or heavy exposure. As two oxidation states of mercury form salts (Hg22+ and Hg2+), mercury salts occur in both mercury(I) (or mercurous) and mercury(II) (mercuric) forms. Mercury(II) salts are usually more toxic than their mercury(I) counterparts because their solubility in water is greater; thus, they are more readily absorbed from the gastrointestinal tract. Mercuric cyanide (also known as Mercury (II) cyanide), Hg(CN)2, is a particularly toxic mercury compound. If ingested, both life-threatening mercury and cyanide poisoning can occur. Hg(CN)2 can enter the body via inhalation, ingestion, or passage through the skin. Inhalation of mercuric cyanide irritates the throat and air passages. 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. Contact with eyes can cause burns and brown stains in the eyes, and long-time exposure can affect the peripheral vision. Contact with skin can cause skin allergy, irritation, and gray skin color. Chronic exposure to trace amounts of the compound can lead to mercury buildup in the body over time; it may take months or even years for the body to eliminate excess mercury. Overexposure to mercuric cyanide can lead to kidney damage and/or mercury poisoning, leading to 'shakes' (ex: shaky handwriting), irritability, sore gums, increased saliva, metallic taste, loss of appetite, memory loss, personality changes, and brain damage. Exposure to large doses at one time can lead to sudden death. Mercuric cyanide has not been tested on its ability to cause reproductive damage. Although inorganic mercury compounds (such as Hg(CN)2) have not been shown to be human teratogens, they should be handled with care, as they are known to damage developing embryos and decrease fertility in men and women. According to one study, two people exhibited symptoms of cyanide poisoning within hours after ingesting mercuric cyanide or mercury oxycyanide, Hg(CN)2•HgO, in suicide attempts. The toxicity of Hg(CN)2 is commonly assumed to arise almost exclusively from mercury poisoning; however, the patient who ingested mercury oxycyanide died after five hours of cyanide poisoning before any mercury poisoning symptoms were observed. The patient who ingested Hg(CN)2 initially showed symptoms of acute cyanide poisoning, which were brought under control, and later showed signs of mercury poisoning before recovering. The degree to which cyanide poisoning occurs is thought to be related to whether cyanide ions are released in the stomach, which depends on factors such as the amount ingested, stomach acidity, and volume of stomach contents. Given that Hg(CN)2 molecules remain undissociated in pure water and in basic solutions, it makes sense that dissociation would increase with increasing acidity. High stomach acidity thus helps cyanide ions to become more bioavailable, increasing the likelihood of cyanide poisoning. Mercury cyanide was used in two murders in New York in 1898. The perpetrator, Roland B. Molineux, sent poisoned medicines to his victims through the US mail. The first victim, Henry Barnett, died of mercury poisoning 12 days after taking the poison. The second victim, Catherine Adams, died of cyanide poisoning within 30 minutes of taking the poison. As in the suicide cases, the difference between the two cases may be attributed to differences in the acidities of the solutions containing the poison, or to differences in the acidities of the victims' stomachs. The drug n-acetyl penicillamine has been used to treat mercury poisoning with limited success. Compounds of mercury tend to be much more toxic than the elemental form, and organic compounds of mercury are often extremely toxic and have been implicated in causing brain and liver damage. The most dangerous mercury compound, dimethylmercury, is so toxic that even a few microliters spilled on the skin, or even a latex glove, can cause death, as in the case of Karen Wetterhahn. Methylmercury is the major source of organic mercury for all individuals. It works its way up the food chain through bioaccumulation in the environment, reaching high concentrations among populations of some species. Top predatory fish, such as tuna or swordfish, are usually of greater concern than smaller species. The US FDA and the EPA advise women of child-bearing age, nursing mothers, and young children to completely avoid swordfish, shark, king mackerel and tilefish from the Gulf of Mexico, and to limit consumption of albacore ("white") tuna to no more than 6 oz (170 g) per week, and of all other fish and shellfish to no more than 12 oz (340 g) per week. A 2006 review of the risks and benefits of fish consumption found, for adults, the benefits of one to two servings of fish per week outweigh the risks, even (except for a few fish species) for women of childbearing age, and that avoidance of fish consumption could result in significant excess coronary heart disease deaths and suboptimal neural development in children. The period between exposure to methylmercury and the appearance of symptoms in adult poisoning cases is long. The longest recorded latent period is five months after a single exposure, in the Dartmouth case (see History); other latent periods in the range of weeks to months have also been reported. No explanation for this long latent period is known. When the first symptom appears, typically paresthesia (a tingling or numbness in the skin), it is followed rapidly by more severe effects, sometimes ending in coma and death. The toxic damage appears to be determined by the peak value of mercury, not the length of the exposure. Ethylmercury is a breakdown product of the antibacteriological agent ethylmercurithiosalicylate, which has been used as a topical antiseptic and a vaccine preservative (further discussed under Thiomersal below). Its characteristics have not been studied as extensively as those of methylmercury. It is cleared from the blood much more rapidly, with a half-life of seven to 10 days, and it is metabolized much more quickly than methylmercury. It is presumed not to have methylmercury's ability to cross the blood–brain barrier via a transporter, but instead relies on simple diffusion to enter the brain. Other exposure sources of organic mercury include phenylmercuric acetate and phenylmercuric nitrate. These were used in indoor latex paints for their antimildew properties, but were removed in 1990 because of cases of toxicity. Diagnosis of elemental or inorganic mercury poisoning involves determining the history of exposure, physical findings, and an elevated body burden of mercury. Although whole-blood mercury concentrations are typically less than 6 μg/L, diets rich in fish can result in blood mercury concentrations higher than 200 μg/L; 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. If the exposure is chronic, urine levels can be obtained; 24-hour collections are more reliable than spot collections. It is difficult or impossible to interpret urine samples of patients undergoing chelation therapy, as the therapy itself increases mercury levels in the samples. Diagnosis of organic mercury poisoning differs in that whole-blood or hair analysis is more reliable than urinary mercury levels. Mercury poisoning can be prevented (or minimized) by eliminating or reducing exposure to mercury and mercury compounds. To that end, many governments and private groups have made efforts to regulate heavily the use of mercury, or to issue advisories about its use. For example, the export from the European Union of mercury and some mercury compounds has been prohibited since 2010-03-15. The variability among regulations and advisories is at times confusing for the lay person as well as scientists. The United States Environmental Protection Agency (EPA) issued recommendations in 2004 regarding exposure to mercury in fish and shellfish. The EPA also developed the "Fish Kids" awareness campaign for children and young adults on account of the greater impact of mercury exposure to that population. Identifying and removing the source of the mercury is crucial. Decontamination requires removal of clothes, washing skin with soap and water, and flushing the eyes with saline solution as needed. Inorganic ingestion such as mercuric chloride should be approached as the ingestion of any other serious caustic. 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. Chelation therapy for acute inorganic mercury poisoning can be done with DMSA, 2,3-dimercapto-1-propanesulfonic acid (DMPS), -penicillamineD (DPCN), or dimercaprol (BAL). Only DMSA is FDA-approved for use in children for treating mercury poisoning. However, several studies found no clear clinical benefit from DMSA treatment for poisoning due to mercury vapor. No chelator for methylmercury or ethylmercury is approved by the FDA; DMSA is the most frequently used for severe methylmercury poisoning, as it is given orally, has fewer side-effects, and has been found to be superior to BAL, DPCN, and DMPS. α-Lipoic acid (ALA) has been shown to be protective against acute mercury poisoning in several mammalian species when it is given soon after exposure; correct dosage is required, as inappropriate dosages increase toxicity. Although it has been hypothesized that frequent low dosages of ALA may have potential as a mercury chelator, studies in rats have been contradictory. Glutathione and -acetylcysteineN (NAC) are recommended by some physicians, but have been shown to increase mercury concentrations in the kidneys and the brain. Experimental findings have demonstrated an interaction between selenium and methylmercury, but epidemiological studies have found little evidence that selenium helps to protect against the adverse effects of methylmercury. Chelation therapy can be hazardous if administered incorrectly. In August 2005, an incorrect form of EDTA used for chelation therapy resulted in hypocalcemia, causing cardiac arrest that killed a five-year-old autistic boy. Many of the toxic effects of mercury are partially or wholly reversible, either through specific therapy or through natural elimination of the metal after exposure has been discontinued. However, heavy or prolonged exposure can do irreversible damage, in particular in fetuses, infants, and young children. Young's syndrome is believed to be a long term consequence of early childhood mercury poisoning. Mercuric chloride may cause cancer as it has caused increases in several types of tumors in rats and mice, while methyl mercury has caused kidney tumors in male rats. The EPA has classified mercuric chloride and methyl mercury as possible human carcinogens (ATSDR, EPA) Mercury may be measured in blood or urine to confirm a diagnosis of poisoning in hospitalized victims or to assist in the forensic investigation in a case of fatal overdosage. Some analytical techniques are capable of distinguishing organic from inorganic forms of the metal. The concentrations in both fluids tend to reach high levels early after exposure to inorganic forms, while lower but very persistent levels are observed following exposure to elemental or organic mercury. Chelation therapy can cause a transient elevation of urine mercury levels. Infantile acrodynia (also known as "calomel disease", "erythredemic polyneuropathy", and "pink disease") is a type of mercury poisoning in children characterized by pain and pink discoloration of the hands and feet. The word is derived from the Greek, where άκρο means end (as in: upper extremity) and οδυνη means pain. Also known as pink disease, Swift disease, Feer disease, Selter disease, erythroderma, erythroderma polyneuritis, dermatopolyneuritis, trophodermatoneurosis, erythema arthricum epidemicum, vegetative neurosis, and vegetative encephalitis. These terms describe different aspects of the syndrome. Acrodynia was relatively commonplace among children in the first half of the 20th century. At first, the cause of the acrodynia epidemic among infants and young children was unknown; however, mercury poisoning, primarily from calomel in teething powders, began to be widely accepted as its cause in the 1950s and 60s. The prevalence of acrodynia decreased greatly after calomel was excluded from most teething powders in 1954. Acrodynia is difficult to diagnose, "it is most often postulated that the etiology of this syndrome is an idiosyncratic hypersensitivity reaction to mercury because of the lack of correlation with mercury levels, many of the symptoms resemble recognized mercury poisoning." Because elemental mercury often passes through the GI tract without being absorbed, it was used medically for various purposes until the dangers of mercury poisoning became known. For example, elemental mercury was used to mechanically clear intestinal obstructions (due to its great weight and fluidity), and it was a key ingredient in various medicines throughout history, such as blue mass. The toxic effects often were either not noticed at all or so subtle or generic that they were attributed to other causes and were not recognized as poisoning caused by mercury. While the usage of mercury in medicine has declined, mercury-containing compounds are still used medically in vaccines and dental amalgam, both of which have been the subject of controversy regarding their potential for mercury poisoning. In 1999, the Centers for Disease Control (CDC) and the American Academy of Pediatrics (AAP) asked vaccine makers to remove the organomercury compound thiomersal (spelled "thimerosal" in the US) from vaccines as quickly as possible, and thiomersal has been phased out of US and European vaccines, except for some preparations of influenza vaccine. The CDC and the AAP followed the precautionary principle, which assumes that there is no harm in exercising caution even if it later turns out to be unwarranted, but their 1999 action sparked confusion and controversy that has diverted attention and resources away from efforts to determine the causes of autism. Since 2000, the thiomersal in child vaccines has been alleged to contribute to autism, and thousands of parents in the United States have pursued legal compensation from a federal fund. A 2004 Institute of Medicine (IOM) committee favored rejecting any causal relationship between thiomersal-containing vaccines and autism. Autism incidence rates increased steadily even after thiomersal was removed from childhood vaccines. Currently there is no accepted scientific evidence that exposure to thiomersal is a factor in causing autism. Dental amalgam, an alloy of about 50 percent elemental mercury, was first introduced in France in the early 19th century. Chosen for its cost-effective durability, this amalgam is a source of low-level exposure to mercury vapour, and an enormous amount of controversy. Although the vast majority of patients with amalgam fillings are exposed to levels believed to be too low to pose any risk to health, many patients (i.e., those in the upper 99.9 percentile) exhibit urine test results that are comparable to those at the maximum allowable legal limits for workplace (occupational) safety. Nonetheless, in the United States the National Institutes of Health has stated that amalgam fillings pose no personal health risk, and that replacement by non-amalgam fillings is not indicated. In Norway, amalgam fillings are banned due to concerns over public health and environmental pollution. In 2002, Maths Berlin, Professor Emeritus of Environmental Medicine and chair of the 1991 World Health Organization Task Group on Environmental Health Criteria for Inorganic Mercury, published][ an overview and assessment of the scientific literature published between November 1997 and 2002 as part of a special investigation for the Swedish Government on amalgam-related health issues. The report concluded: "With reference to the fact that mercury is a multipotent toxin with effects on several levels of the biochemical dynamics of the cell, amalgam must be considered to be an unsuitable material for dental restoration." Some skin whitening products contain the toxic chemical mercury(II) chloride as the active ingredient. When applied, the chemical readily absorbs through the skin into the bloodstream. The use of mercury in cosmetics is illegal in the United States. However, cosmetics containing mercury are often illegally imported. Following a certified case of mercury poisoning resulting from the use of an imported skin whitening product, the United States Food and Drug Administration warned against the use of such products. Symptoms of mercury poisoning have resulted from the use of various mercury-containing cosmetic products. The use of skin whitening products is especially popular amongst Asian women. In Hong Kong in 2002, two products were discovered to contain between 9,000 to 60,000 times the recommended dose. Fluorescent lamps contain mercury which is released when bulbs are broken. Mercury in bulbs is typically present as either elemental mercury liquid, vapor, or both, since the liquid evaporates at ambient temperature. When broken indoors, bulbs may emit sufficient mercury vapor to present health concerns, and the U.S. Environmental Protection Agency recommends evacuating and airing out a room for at least 15 minutes after breaking a fluorescent light bulb. Breakage of multiple bulbs presents a greater concern. A 1987 report described a 23-month-old toddler who suffered anorexia, weight loss, irritability, profuse sweating, and peeling and redness of fingers and toes. This case of acrodynia was traced to exposure of mercury from a carton of 8-foot fluorescent light bulbs that had broken in a potting shed adjacent to the main nursery. The glass was cleaned up and discarded, but the child often used the area for play. Mercury has been used at various times to assassinate people. In 2008, Russian lawyer Karinna Moskalenko claimed to have been poisoned by mercury left in her car, while in 2010 journalists Viktor Kalashnikov and Marina Kalashnikova accused Russia's FSB of trying to poison them. M: TOX gen / txn pto ant
Poison oak is a deciduous shrub native to North America. Its leaves contain a compound that causes a rash on human skin. Poison oak can specifically refer to: Poison oak (Toxicodendron diversilobum) and its eastern counterpart poison ivy (T. radicans) are two of the North American plants most painful to humans. Note: These species were formerly placed in the genus Rhus. Poison oak and a related, look-alike shrub, Rhus trilobata belong to the sumac family (Anacardiaceae). Poison oak is widespread throughout the mountains and valleys of California. It thrives in shady canyons and riparian habitats. It commonly grows as a climbing vine with aerial (adventitious) roots that adhere to the trunks of oaks and sycamores. Rocky Mountain poison oak (Toxicodendron rydbergii) occurs in canyons throughout the western United States and Canada. Because the two species of western poison oak look like a vine as they develop, some authors list poison oak as a subspecies of eastern poison ivy. Poison oak often grows like a climbing vine. The cautionary rhyme "leaves of three, let it be" applies to poison oak, as well as to )Toxicodendron radicanspoison ivy (.
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