Lead poisoning is a type of metal poisoning caused by lead in the body. The brain is the most sensitive. Symptoms may include abdominal pain, constipation, headache, irritability, memory problems, inability to have children, and tingling in the hands and feet. This accounts for nearly 10% of intellectual disability as an unknown cause and can cause behavioral problems. Some of the effects are permanent. In severe cases, anemia, seizures, coma, or death may occur.
Exposure to lead can occur by contaminated air, water, dust, food, or consumer products. Children have a greater risk because they are more likely to place objects in their mouths such as those containing lead paint and absorb a greater proportion of the lead they eat. Occupational exposure is a common cause of lead poisoning in adults with certain occupations at particular risk. Diagnosis is usually based on measurement of blood lead levels. The Centers for Disease Control (US) has set an upper limit for lead blood for adults at 10 Ã,Âμg/dl (10 Âμg/100 g) and for children at 5 Ã,Âμg/dl. Increased lead can also be detected by changes in red blood cells or solid lines in the bones of children as seen on X-rays.
Lead poisoning can be prevented. This includes individual efforts such as removing items that contain lead from home, workplace efforts such as increased ventilation and monitoring, and national policies such as laws prohibiting lead in products such as paint and gasoline, reducing the allowable levels in water or soil, and provide to clean contaminated soil. The primary treatment is the removal of lead sources and the use of lead-binding drugs that can be removed from the body, known as chelation therapy. Chelation therapy in children is recommended when the blood level is greater than 40-45 Âμg/dl. Medications used include dimercaprol, edetate calcium disodium, and succimer.
In 2013 the lead is believed to have generated 853,000 deaths. This is most common in developing countries. The poor have a greater risk. Lead is believed to produce 0.6% of the world's disease burden. People have been mining and using tin for thousands of years. Description of the date of lead poisoning up to at least 2000 BC, while attempts to limit the date of use of lead back at least in the 16th century. Concerns for low exposure levels began in the 1970s with no safe threshold for lead exposure.
Video Lead poisoning
Classification
Classically, "lead poisoning" or "lead poisoning" has been defined as high lead exposure that is usually associated with severe health effects. Poisoning is a symptom pattern that occurs with toxic effects from medium to high exposure levels; toxicity is a broader spectrum of effects, including subclinical ones (which do not cause symptoms). However, professionals often use "lead poisoning" and "lead poisoning" interchangeably, and official sources do not necessarily limit the use of "lead poisoning" to refer only to the symptomatic effects of lead.
The amount of lead in blood and tissue, as well as time of exposure, determines toxicity. Lead poisoning may be acute (from intense short duration) or chronic (from repeated low-level exposure during prolonged periods), but the latter is much more common. Diagnosis and treatment of lead exposure is based on the level of lead in the blood (the amount of lead in the blood), measured in micrograms of lead per deciliter of blood (? G/dL). The level of lead in water can also be used, albeit less frequently. In the case of exposure to chronic exposure, frequent secretion occurs in the first highest concentration of bone, then in the kidneys. If the provider does a provocative excretion test, or "chelation challenge," measurements obtained from urine rather than blood tend to provide a more accurate representation of total lead load to a skilled translator.
The US Centers for Disease Control and Prevention and World Health Organization states that a blood lead level of 10 g/dL or above is a cause for concern; however, lead can impair development and have harmful health effects even at lower levels, and no known level of exposure is safe. Authorities such as the American Academy of Pediatrics define lead poisoning as blood lead levels higher than 10 g/dL.
Lead forms various compounds and exists in environments in various forms. The poisoning feature varies depending on whether the agent is an organic (carbonaceous), or an inorganic compound. Organic lead poisoning is now very rare, as countries around the world have stopped using organic lead compounds as petrol additives, but they are still used in industrial settings. Organic lead compounds, which cross skin and respiratory tract easily, affect the central nervous system predominantly.
Maps Lead poisoning
Signs and symptoms
Lead poisoning can cause various symptoms and signs that vary depending on the individual and the duration of lead exposure. The symptoms are not specific and may be subtle, and a person with high lead levels may not have symptoms. Symptoms usually develop for weeks for months because of deposits in the body during chronic exposure, but acute symptoms of brief and intense exposure also occur. Symptoms of organic lead exposure, which may be more toxic than inorganic lead because of its fat solubility, occur rapidly. Poisoning by organic lead compounds has major symptoms in the central nervous system, such as insomnia, delirium, cognitive deficits, tremor, hallucinations, and seizures.
Symptoms may differ in adults and children; the main symptoms in adults are headache, stomach pain, memory loss, kidney failure, male reproductive problems, and weakness, pain, or tingling in the extremities.
Early symptoms of lead poisoning in adults are usually non-specific and include depression, loss of appetite, intermittent abdominal pain, nausea, diarrhea, constipation, and muscle aches. Other early signs in adults include malaise, fatigue, decreased libido, and problems with sleep. Unusual flavors in the mouth and personality changes are also early signs.
In adults, symptoms can occur at levels above 40 Âμg/dL, but more likely to occur only above 50-60? G/dL. Symptoms begin to appear in children generally around 60 Âμg/dL. However, the level of lead in which the symptoms appear varies greatly depending on the unknown characteristics of each individual. At lead levels in the blood between 25 and 60? G/dL, neuropsychiatric effects such as delayed reaction time, irritability, and difficulty concentrating, as well as delayed motor neuronal conduction and headaches may occur. Anemia can appear at blood lead levels higher than 50 Âμg/dL. In adults, colic stomach, which involves paroxysms of pain, can appear at a blood lead level greater than 80 Âμg/dL. Signs that occur in adults at the level of lead in the blood exceed 100 g/dL including decreased wrist and foot fall, and signs of encephalopathy (conditions characterized by swelling of the brain), such as those accompanying increased pressure inside the skull, delirium, coma, seizures, and headaches. In children, signs of encephalopathy such as strange behavior, discoordination, and apathy occur at lead levels exceeding 70 Âμg/dL. For adults and children, it is rarely asymptomatic if blood lead levels exceed 100 Âμg/dL.
Acute poisoning
In acute poisoning, the typical neurological signs are pain, muscle weakness, numbness and tingling, and, rarely, symptoms associated with brain inflammation. Abdominal pain, nausea, vomiting, diarrhea, and constipation are other acute symptoms. The effects of tin on the mouth include astringency and metal taste. Gastrointestinal problems, such as constipation, diarrhea, poor appetite, or weight loss, are common in acute poisoning. Large amounts of tin absorption in a short time can cause shock (insufficient fluid in the circulatory system) due to water loss from the gastrointestinal tract. Hemolysis (rupture of red blood cells) due to acute poisoning can cause anemia and hemoglobin in the urine. Kidney damage can cause changes in urination such as decreased urine output. Survivors of acute poisoning often show symptoms of chronic poisoning.
Chronic poisoning
Chronic toxicity usually presents with symptoms that affect some systems, but is associated with three main types of symptoms: gastrointestinal, neuromuscular, and neurological. Central nervous system and neuromuscular symptoms are usually produced from intense exposure, whereas gastrointestinal symptoms usually result from exposure in longer periods. Signs of chronic exposure include short-term memory loss or concentration, depression, nausea, abdominal pain, loss of coordination, and numbness and tingling in the extremities. Fatigue, sleep problems, headache, fainting, slurred speech, and anemia are also found in chronic lead poisoning. The "main hue" of the skin with pallor and/or lividity is another feature. The blue line along the chewing gum with the bluish black rims on the teeth, known as the 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. Visual disturbance can occur with gradual blurred vision as a result of central scotoma, caused by toxic optic neuritis.
Effects on children
A woman who has high blood lead levels during pregnancy is at greater risk of preterm delivery or low birth weight. Children are at increased risk of lead poisoning because their smaller bodies are in a state of continuous growth and development. Lead is absorbed at a faster rate than adults, which causes more physical damage than older people. In addition, children, especially when they learn to crawl and walk, are constantly on the floor and therefore more susceptible to swallowing and inhaling dust contaminated with lead.
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 developments of normal childhood behavior, such as speaking and using words, and permanent intellectual disabilities are often seen. Although less common, it is possible to nail to develop leukonychia striata if exposed to abnormally high lead concentrations.
With the organ system
Lead affects every organ system of the body, 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 associated with lead exposure, such as cataracts. Exposure to intrauterine and neonate lead promotes tooth decay. Apart from the unique developmental effects for children, the health effects experienced by adults are similar to those in children, although the threshold is generally higher.
Kidney
Kidney damage occurs with high tin exposure, and evidence suggests that lower levels can damage the kidneys as well. The toxic effects of lead cause nephropathy and can cause Fanconi syndrome, in which renal proximal tubular function is impaired. Longer-term exposures to lower levels than those causing lead nephropathy have also been reported as nephrotoxic in patients from developed countries who have chronic kidney disease or are at risk due to hypertension or diabetes mellitus. Lead poisoning inhibits urating excretion of waste products and leads to a predisposition for gout, where the tendon is formed. This condition is known as saturnine gout .
Cardiovascular system
Evidence suggests lead exposure is associated with high blood pressure, and the study also found an association between lead exposure and coronary heart disease, heart rate variability, and stroke death, but the evidence is more limited. People who have been exposed to higher lead concentrations may have a higher risk for autonomic cardiac dysfunction in days when ozone and fine particles are higher.
Reproductive System
Lead affects the male and female reproductive systems. In men, when blood lead levels exceed 40 Âμg/dL, sperm counts are reduced and changes occur in sperm volume, their motility, and their morphology. Increased lead levels in the blood of pregnant women can cause 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 both mother and baby are usually the same. The fetus may be poisoned in utero if the lead from the mother's bone is then mobilized by metabolic changes due to pregnancy; increased intake of calcium in pregnancy may help reduce this phenomenon.
Nervous system
Lead affects the peripheral nervous system (especially the motor nerves) and the central nervous system. The effects of the peripheral nervous system are more prominent in adults and the effects of the central nervous system are more prominent in children. Lead causes the axons of nerve cells to degenerate and lose their mielin coats.
Lead exposure in young children has been linked to learning disabilities, and children with lead concentrations in the blood greater than 10 g/dL are in danger of developmental disabilities. Increased blood lead levels in children have been correlated with decreased intelligence, nonverbal reasoning, short-term memory, attention, reading and arithmetic skills, fine motor skills, emotional regulation, and social engagement.
The influence of lead on the cognitive abilities of children occurs at very low levels. There appears to be no lower limit for dose-response relationships (unlike other heavy metals such as mercury). The decrease in academic achievement has been associated with lead exposure even in blood lead levels lower than 5 g/dL. Blood lead levels below 10 Âμg/dL have been reported to be associated with low IQ and behavioral problems such as aggression, proportional to blood lead levels. Between 5 and 35 Âμg/dL blood lead levels, an IQ reduction of 2-4 points for each increase in g/dL was reported in children. However, studies showing the relationship between low-grade lead exposure and health effects in children may be affected by bullies and overstate the effects of low-grade lead exposure.
High blood lead levels in adults are also associated with a decrease in cognitive performance and with psychiatric symptoms such as depression and anxiety. Found in a large group of inorganic and inorganic lead workers currently in Korea that the level of lead blood in the range of 20-50? G/dL correlates with neuro-cognitive defects. Increases in blood lead levels from about 50 to about 100 g/dL in adults have been found to be associated with impaired functioning of the central nervous system that is persistent, and possibly permanent.
Lead exposure in children is also correlated with neuropsychiatric disorders such as attention deficit hyperactivity disorder and anti-social behavior. Increased lead levels in children correlate with higher scores on aggression and delinquency measures. Correlations have also been found between prenatal and early childhood exposure and violent crime in adulthood. Countries with the highest levels of air lead have also been found to have the highest murder rates, after adjusting for confounding factors. A May 2000 study by economic consultant Rick Nevin theorized that lead exposure accounts for 65% to 90% of variation in violent crime rates in the US. A 2007 paper by the same authors claims to show a strong relationship between preschool bloodstream and subsequent trend-level crime for decades in nine countries. Exposure to lead in childhood appears to increase school suspensions and juvenile detention among boys. It is believed that the US ban on lead paint in buildings in the late 1970s, as well as the termination of leaded gasoline in the 1970s and 1980s, has partially helped contribute to the decline of violent crime in the United States since the early 1990s.
Exposure route
Lead is a common environmental pollutant. Causes of environmental contamination include industrial tin usage, such as found in facilities that process lead-acid batteries or produce lead or pipe wire, and metal recycling and metal casting. Battery storage and ammunition are made with the largest amount of lead consumed in the economy each year, in the US by 2013. Children living near lead-in-process facilities, such as lead smelting, have been found to have very high levels of lead in the blood. In August 2009, parents rioted in China after lead poisoning was found in nearly 2,000 children living near zinc and manganese smelting. Lead exposure can occur from contact with lead in the air, household dust, soil, water, and commercial products. Lead gas is also associated with increased lead pollution. Several studies have shown a link between leaded gasoline and crime rates. Man-made tin contamination has been rising in the air over the past 2000 years. Lead pollution in the air is entirely due to human activities (mining and smelting).
Work exposure
In adults, occupational exposure is a major cause of lead poisoning. People can be exposed while working in a facility that produces a variety of lead-containing products; These include radiation shields, ammunition, certain surgical equipment, developing a dental x-ray film before digital x-rays (each packet has a lead liner to prevent radiation through), fetal monitor, plumbing, circuit board, jet engine, and ceramic glaze. In addition, miners and lead smelting, plumbers and builders, automobile mechanics, glass manufacturers, construction workers, battery and recycler manufacturers, shotgun instructors, and plastic manufacturers are at risk of lead. Other work that presents the risk of lead exposure include welding, rubber making, printing, zinc and copper smelting, ore processing, solid waste combustion, and paint and pigment production. Tin-exposed parents at work can bring dust back to their clothes or skin and expose their children. Occupational exposure to lead increases the risk of cardiovascular disease, particularly: stroke, and high blood pressure.
Food
Lead can be found in foods when food grows in high lead soil, lead in the air pollutes plants, feeding animals lead in their food, or leads into food either from what is stored or cooked.
Cat
Some lead compounds are colorful and widely used in paints, and lead paint is the main route of lead exposure in children. A study conducted in 1998-2000 found that 38 million house units in the US had lead-based paint, down from the 1990 estimate of 64 million. Deteriorating lead paint can produce dangerous levels of lead in dust and domestic soil. Deteriorating lead paint and household dust containing lead are the main causes of chronic lead poisoning. Tin decomposes into dust and because children are more vulnerable to crawling on the floor, it is easily digested. Many children show pica, eat things that are not food. Even small amounts of lead-containing products such as paint chips or a glaze can contain dozens or hundreds of milligrams of lead. Consuming lead paint flakes creates special hazards for children, generally resulting in more severe poisoning than those from dust. For removing lead paint from the dwelling, eg. with sanding or burning creating lead dust and smoke, it is generally safer to seal lead paint under new paint (except moving windows and doors, which create paint dust when operated). Alternately, special precautions should be taken if lead paint should be removed. In oil paintings it was once common for colors like yellow or white to be made with carbonate lead. Leading color white oil is a major white oil painter until it is replaced by zinc or titanium-containing compounds in the mid-20th century. It is speculated that the Caravaggio painter and perhaps Francisco Goya and Vincent Van Gogh have caused poisoning due to overexposure or carelessness when handling this color.
Land
The remaining tin on the ground contributes to lead exposure in urban areas. It is estimated that the more polluting an area with various contaminants, the more likely it is to have lead. However, this is not always the case, as there are several other reasons for lead contamination in the soil. The content of lead in the soil may be caused by faulty lead paint, residues from lead-containing gasoline, used engine oil, tire weights, or pesticides used in the past, contaminated landfills, or from nearby industries such as foundry or fuser. Although leaded soil is less of a problem in countries that no longer have lead, but remains a commonplace, raising concerns about the security of urban agriculture; eating foods grown on contaminated soil may pose a danger of lead.
Water
Lead from the atmosphere or soil may end up in ground water and surface water. It is also potentially in drinking water, for example from pipes and fixtures made of lead or lead solder. Since acid water breaks lead in pipes more easily, chemicals can be added to municipal water to increase pH and thereby reduce corrosivity of public water supplies. Chlorine, which is adopted as a substitute for chlorine disinfectant due to fewer health problems, increases corrosion. In the US, 14-20% of total lead exposure is associated with drinking water. In 2004, a team of seven journalists from The Washington Post found a high level of lead in drinking water in Washington, D.C. and won an award for an investigative report for a series of articles on this contamination. In the Flint water crisis, the transition to more corrosive urban water sources increases lead levels in drinking water in domestic tap water.
Collecting rainwater from roof runoff that is used as drinking water can contain lead if there is lead contaminants in the roof or in storage tanks. The Australian Drinking Water Guidelines allow a maximum of 0.01 mg/L of lead in water.
Products containing lead
Lead can be found in products such as kohl, ancient cosmetics from the Middle East, South Asia, and parts of Africa that have many names; and from some toys. In 2007, millions of Chinese-made toys were withdrawn from various countries due to security hazards including lead paint. Vinyl mini-blinds, found mainly in older housing, may contain lead. Lead is generally incorporated into herbal remedies such as Indian Ayurvedic preparations and Chinese medicine. There is also a risk of increased blood lead levels caused by traditional medicines such as azarcon and greta , each containing about 95% tin.
Ingestion of metal tin, such as small fishing lures, increases lead levels in the blood and can be fatal. Eating food that is contaminated with lead is also a threat. Ceramic glaze often contains lead, and dish that has been dismissed incorrectly can soak metal into food, potentially causing severe poisoning. In some places, the solder in the tin used for food contains lead. When making medical equipment and hardware, lead-containing solder may be present. People who eat animals hunted with tin bullets may be at risk of lead. Bullets placed in the body rarely lead to significant levels of lead, but bullets lodged in the joint are exceptions, as the bullets get worse and release lead into the body over time.
In May 2015, India's food safety regulator in Uttar Pradesh state found that the Mie 2 MI Maggi sample contains lead up to 17 times exceeding the permitted limits. On June 3, 2015, the New Delhi Government banned the sale of Maggi noodles in New Delhi stores for 15 days because they found containing tin beyond the permitted limits. The Gujarat FDA on June 4, 2015 banned noodles for 30 days after 27 of 39 samples were detected with unpleasant metal tin levels, among others. Some of India's biggest retailers such as Future Group, Big Bazaar, Easyday, and Nilgiris have imposed a national ban on Maggi noodles. Many other countries have also banned the Maggi noodles.
Bullet
Contact with ammunition is the source of lead exposure. In 2013, lead-based munitions production is the second largest annual use of tin in the US, accounting for more than 84,800 metric tons consumed in 2013. second after storage battery manufacture. The Environmental Protection Agency (EPA) can not manage cartridges and shells, as a matter of law. Birdshot is banned in some areas, but this is primarily for birds and predators, not humans. Contamination of the various weapons used is a concern for those living close by. Non-lead alternatives include steel, tungsten-nickel-iron, bismuth-tin, and tungsten-polymers.
Because game animals can be shot using tin bullets, the potential for lead consumption from milled meat consumption has been studied clinically and epidemiologically. In a recent study conducted by the CDC, groups from North Dakota were registered and asked to self-report the historical consumption of game meat, and participation in other activities that could lead to lead exposure. The study found that age, sex, age of housing, current hobbies with potential lead exposure, and consumption of the game are all related to blood lead levels (PbB).
According to a study published in 2008, 1.1% of the 736 people who consumed wild animal meat tested had PbB> = 5 g/dl In November 2015 the US HHS/CDC/NIOSH was set at 5 Âμg/dL (five micrograms per decyliters) of all blood, in venous blood samples, as reference reference blood levels for adults. The elevated BLL is defined as BLL> = 5 Âμg/dL. The definition of the case is used by the ABLES program, State Council and Territorial Epidemiology (CSTE), and the CDC's Verified National Disease Control System (NNDSS). Previous (ie from 2009 to November 2015), the case definition for high BLL is BLL> = 10 Âμg/dL.
Copper-based and jacketed bullets are more economical to produce and use than lead or other materials. Alternative materials are available such as steel, copper, and tungsten, but alternatives are universally less effective and/or more expensive. However, the biggest obstacle to using most of the alternatives relates to current legislation in the United States relating to armor-piercing rounds. Laws and regulations relating to ammunition penetrating armor strictly prohibit the use of brass, bronze, steel, tungsten, and almost every metal alternative in bullet that can be shot with a gun, which is currently almost every caliber smaller than 50BMG (including the popular remington 0.223 ,.308 Winchester and.30-06 to name just a few). Some bullet-based bullets are resistant to fragmentation, offering hunters the ability to clean game animals with negligible risks including lead fragments in prepared meat. Other bullets are vulnerable to fragmentation and exacerbate the risk of lead ingestion from processed meats. In practice, the use of unbroken bullets and proper cleansing of the game's wounds can remove the risk of ingestion of lead from consuming the game; However, isolating the practice to experimentally determine its relationship to lead levels in difficult research. Bismuth is an element used as a major replacement for gun pellets used in waterfowl hunting even though the shotshell made of bismuth is almost ten times more expensive than lead.
Pathophysiology
Exposure occurs through inhalation, ingestion or occasional skin contact. Lead can be taken by direct contact with the mouth, nose, and eyes (mucous membranes), and through resting on the skin. Tetraethyllead, which is a gasoline additive and still used in fuels such as aviation fuel, passes through the skin; but the inorganic tin found in paints, food, and most consumer products containing lead is only absorbed minimally through the skin. The main source of absorption of inorganic lead comes from consumption and inhalation. In adults, about 35-40% of inhaled inhaled dust is stored in the lungs, and about 95% of those entering the bloodstream. Of the digestible inorganic tin, about 15% is absorbed, but this percentage is higher in children, pregnant women, and people with calcium, zinc, or iron deficiency. Infants can absorb about 50% of the ingested lead, but little is known about the rate of absorption in children.
The main body compartments that store lead are blood, soft tissue, and bone; the lead beak in this tissue is measured in weeks for blood, months for soft tissue, and years for bone. Leads in bones, teeth, hair, and nails are tightly bound and not available to other tissues, and are generally considered harmless. In adults, 94% of the absorbed lead is stored in bones and teeth, but children save only 70% this way, a fact that some can explain the more serious health effects in children. The estimated half-life of lead in the bone is 20 to 30 years, and the bone can enter the lead into the bloodstream long after the initial exposure is lost. The lead half life in men is about 40 days, but may be longer in children and pregnant women, whose bones are remodeling, allowing lead to be continuously reintroduced into the bloodstream. Also, if lead exposure lasts for years, the distance is much slower, partly because of the return of lead from the bone. Many other tissues store lead, but those with the highest concentrations (other than blood, bones, and teeth) are the brain, spleen, kidneys, liver, and lungs. Lead is removed from the body very slowly, mainly through urine. A small amount of lead is also removed through the stool, and a very small amount in hair, nails, and sweat.
Lead has no relevant physiological role in the body, and its harmful effects are numerous. Lead and other heavy metals create reactive radicals that damage cell structures including DNA and cell membranes. Lead also interferes with DNA transcription, an enzyme that helps in the synthesis of vitamin D, and enzymes that maintain the integrity of cell membranes. Anemia can occur when the red cell membrane becomes more brittle as a result of damage to the membrane. It interferes with bone and teeth metabolism and alters the permeability of blood vessels and collagen synthesis. Lead can also damage the developing immune system, leading to excessive production of inflammatory proteins; this mechanism can mean that lead exposure is a risk factor for asthma in children. Lead exposure is also associated with decreased activity of immune cells such as polymorphonuclear leukocytes. Lead also disrupts the normal metabolism of calcium in the cell and causes it to form in it.
Enzyme
The main cause of lead toxicity is interference with various enzymes because it binds to the sulfhydryl groups found in many enzymes. The lead toxicity part results from its ability to mimic other metals that take part in biological processes, which act as cofactors in many enzymatic reactions, replacing them in the enzymes in which they act. Lead is able to bind and interact with many of the same enzymes as this metal but, due to different chemistry, does not work as well as a cofactor, thus interfering with the ability of the enzyme to catalyze its normal reaction or reaction. Among the important metals that interact with tin are calcium, iron, and zinc.
The lead ion has a pair of free electrons in its electronic structure, which can produce distortion in ligand coordination, and in 2007 hypothesized to be important in the effect of lead poisoning on the enzyme (see Lone pair ç§ Unusual self-pair).
One of the main causes of lead pathology is that it interferes with the activity of an essential enzyme called delta-aminolevulinic acid dehydratase, or ALAD (see image of enzyme structure), 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 protoporfirin and Fe 2 to form heme. Lead interference with heme synthesis results in the production of zinc protoporphyrin and the development of anemia. Another effect of lead interference with heme synthesis is the accumulation of heme precursors, such as aminolevulinic acid, which may be directly or indirectly harmful to neurons.
Neuron
The brain is the organ that is most sensitive to lead exposure. Lead is able to pass through the endothelial cells in the blood brain barrier as it can replace calcium ions and be startled by the calcium-ATPase pump. Lead poisoning impairs the normal development of the child's brain and nervous system; therefore children are at greater risk of lead neurotoxicity than adults. In a developing child's brain, lead affects the formation of synapses in the cerebral cortex, neurochemical development (including neurotransmitters), and ion channel arrangement. This results in loss of myelin neuron sheath, reduces the number of neurons, interferes with neurotransmission, and reduces neuronal growth.
Lead-ions (Pb 2 ), such as magnesium-ion (Mg 2 ), block NMDA receptors. Since normal concentrations of Pb 2 in low extracellular fluids (adult average of 120 mg), even a low concentration of Pb 2 has a significant positive effect on the blockage of NMDA receptors. Therefore, increased concentrations of Pb 2 , will, effectively, inhibit the long-term potential (LTPs), and cause long-term abnormal depression (LDP) increases in neurons in the affected part of the system nerve. This disorder leads to the downregulation of NMDA receptors indirectly, effectively initiating a positive feedback loop for LDP. Targeting NMDA receptors is considered to be one of the major causes of lead toxicity to neurons.
Diagnosis
The diagnosis includes determining clinical signs and medical history, with investigation of possible routes of exposure. Clinical toxicology, a medical specialist in the field of poisoning, may be involved in diagnosis and treatment. The main tool in diagnosing and assessing the severity of lead poisoning is the laboratory analysis of blood lead levels (BLL).
Blood film examination may reveal the formation of basophilic red blood cells (dots in red blood cells seen through a microscope), as well as changes typically associated with iron-deficiency anemia (micrositosis and hypochromasia). This may be known as sideroblastic anemia. However, basophilic stippling is also seen in unrelated conditions, such as megaloblastic anemia caused by vitamin B12 (colbalamin) and folate deficiency. Contrary to other sideroblastic anemia, however, there is no sideroblast ring in bone marrow removal.
Lead exposure can also be evaluated by measuring the protoporphyrin erythrocytes (EP) in blood samples. EP is a part of red blood cells that is known to increase as the amount of lead in the blood is high, with a delay of several weeks. Thus the EP level in relation to blood lead levels can suggest a time period of exposure; If blood lead levels are high but EP is still normal, these findings show recent exposure. However, EP levels alone are not sensitive enough to identify high blood lead levels below about 35 Âμg/dL. Because of higher thresholds for detection and the fact that EP levels also increase iron deficiency, the use of this method to detect lead exposure has decreased.
The level of blood lead is an indicator especially new or current lead exposure, rather than total body weight. Lead in bone can be measured noninvasively by X-ray fluorescence; this may be the best measure of cumulative exposure and total body weight. However, this method is not widely available and is primarily used for research rather than routine diagnosis. Another radiographic sign of high lead levels is the presence of a radiodene line called the tin line on the metaphysis of the long bones of growing children, especially around the knee. These major lines, caused by increased calcification due to impaired metabolism of the growing bone, become wider as the increase in lead exposure. X-rays may also reveal tin-containing foreign materials such as paint chips in the gastrointestinal tract.
The fecal lead content measured over several days may also be an accurate way to estimate the overall amount of lead intake of childhood. This form of measurement can serve as a useful way of looking at the extent of oral lead exposure from all food and environmental sources from lead.
Lead poisoning shares symptoms with other conditions and may be easily missed. The conditions present are the same and should be ruled out in diagnosing lead poisoning including carpal tunnel syndrome, Guillain-Barrà © Å syndrome, renal colic, appendicitis, adult encephalitis, and viral gastroenteritis in children. Other differential diagnoses in children include constipation, abdominal colic, iron deficiency, subdural hematoma, central nervous system neoplasm, emotional and behavioral disorders, and intellectual disabilities.
Reference level
The current reference range for acceptable blood lead concentration in healthy people without excessive exposure to lead sources is less than 5 Âμg/dL for children. That's less than 25 Ã,Âμg/dL for adults. Before 2012 the value for children is 10 (Âμg/dl). The current biological exposure index (levels not exceeded) for exposure workers in the US is 30 Âμg/dL in random blood specimens.
In 2015, US HHS/CDC/NIOSH is set 5 Âμg/dL (five micrograms per deciliter) of whole blood, in venous blood samples, as reference reference blood levels for adults. The elevated BLL is defined as BLL> = 5 Âμg/dL. The definition of the case is used by the ABLES program, State Council and Territorial Epidemiology (CSTE), and the CDC's Verified National Disease Control System (NNDSS). Previous (ie from 2009 to November 2015), the case definition for high BLL is BLL> = 10 Âμg/dL. The national geometric BLL meanings among adults is 1.2? G/dL in 2009-2010.
The concentration of lead in the blood of poisoning victims ranged from 30- & gt; 80 μg/dL in children exposed to lead paint in older homes, 77-104 Âμg/dL in people working with glaze pottery, 90-137 Âμg/dL in individuals consuming contaminated herbal medicines, 109- 139 Âμg/dL in indoor shooting instructor and as high as 330 Âμg/dL in those who drank fruit juice from pottery glass containers.
Prevention
In many cases, lead poisoning can be prevented by avoiding lead exposure. Prevention strategies can be divided into individuals (actions taken by the family), preventive treatment (identifying and intervening with high-risk individuals), and public health (reducing risks at the population level).
Measures suggested by individuals to reduce lead levels in the blood of children include increasing the frequency of hand washing and their calcium and iron intake, making them reluctant to put their hands to their mouths, vacuum frequently, and eliminate the presence of objects which contains lead such as curtains and jewelry at home. At home with lead pipes or plumbing, this can be replaced. Less permanent but less expensive methods include water flowing in the morning to water the most contaminated water, or adjust water chemistry to prevent corrosion of pipes. The lead test apparatus is commercially available to detect the presence of lead in the household. Since hot water is more likely than cold water to contain more lead, use only cold water from the tap for drinking, cooking, and for making formula milk. Since most lead in household water usually comes from pipes at home and not from local water supplies, using cold water can avoid lead exposure. Measures such as dust control and household education appear to be ineffective in altering the blood levels of children.
Screening is an important method in prevention treatment strategies. A screening program exists to test the blood of high-risk children for lead exposure, such as those living near lead-related industries.
Preventive measures also exist at the national and city levels. Recommendations by healthcare professionals to reduce childhood exposures include prohibiting the use of lead in unimportant places and strengthening regulations that limit the amount of lead in soil, water, air, household dust, and products. The rules exist to limit the amount of lead in paints; for example, the law of 1978 in the US limits lead in paint for dwellings, furniture, and toys to 0.06% or less. In October 2008, the US Environmental Protection Agency reduced allowable lead levels by a factor of ten to 0.15 micrograms per cubic meter of air, giving the country five years to comply with standards. EU Hazard Age Restrictions The guidelines limit the number of lead and other toxic substances in electronics and electrical appliances. In some places, remediation programs exist to reduce the presence of lead when found high, for example in drinking water. As a more radical solution, entire towns located near major mine sites have been "closed down" by the government, and populations are resettled elsewhere, as is the case with Picher, Oklahoma in 2009.
Treatment
The primary treatment is removal from lead sources and, for people who have high blood lead levels significantly or who have symptoms of poisoning, chelation therapy. Treatment of iron, calcium, and zinc deficiency, which is associated with an increase in lead uptake, is another part of the treatment for lead poisoning. When lead-containing material is present in the gastrointestinal tract (as evidenced by abdominal X-rays), all intestinal irrigation, catharsis, endoscopy, or even surgical removal may be used to remove it from the gut and prevent further exposure. Bullets and shrapnel containing lead can also be a threat of further exposure and may have to be removed surgically if they are in or near a fluid or synovial space. If lead encephalopathy is present, anticonvulsants may be given to control seizures, and treatments to control brain swelling include corticosteroids and mannitol. The treatment of organic lead poisoning involves removal of lead compounds from the skin, preventing further exposure, curing seizures, and possibly chelation therapy for people with high blood lead concentrations.
The chelating agent is a molecule with at least two negatively charged groups that allow it to form complexes with metal ions with a double positive charge, such as lead. The formed fibers are non-toxic and can be excreted in the urine, initially up to 50 times the normal number. The chelating agents used for the treatment of lead poisoning are disodium edetate (CaNa 2 EDTA), dimercaprol (BAL), injected, and succimer and d-penicillamine, 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 Âμg/dL. While the use of chelation for people with lead poisoning symptoms is widely supported, use in asymptomatic people with high blood lead levels is more controversial. Chelation therapy has limited value for cases of chronic exposure at low lead levels. Chelation therapy usually stops when symptoms disappear or when blood lead levels return to the premorbid level. When lead exposure has occurred in the long term, blood lead levels may increase after chelation is stopped because lead is scattered to the blood from the store on the bone; such repeated treatments are often necessary.
Persons receiving embolism should be assessed for peanut allergy because commercial formulations contain peanut oil. Calcium EDTA is also effective if given four hours after administration is treated. Administration, DMSA (Succimer), or DMPS before EDTA calcium is required to prevent redistributing lead into the central nervous system. Self-impregnated use can also redistribute it to the brain and testes. Adverse side effects of calcium EDTA are renal toxicity. Succimer (DMSA) is the preferred agent in the case of mild to moderate lead poisoning. This may occur in cases where children have a level of blood lead & gt; 25? G/dL. The most reported side effect for succimers is gastrointestinal disorders. It is also important to note that chelation therapy only lowers blood lead levels and may not prevent lead-related cognitive problems associated with lower lead levels in the tissues. This may be due to the inability of these agents to remove enough lead from the network or the inability to reverse pre-existing damage. Chelating agents can have adverse effects; for example, chelation therapy can decrease the body's nutritional levels such as zinc. Chelating agents taken orally can increase absorption of lead through the gut.
Chelation challenges, also known as provocation tests, are used to indicate a high body weight and easily move from heavy metals including lead. This test involves collecting urine before and after dosing a single chelating agent to mobilize heavy metals into the urine. The urine is then analyzed by the laboratory for heavy metal content; from this analysis, the overall body weight is inferred. Chelation challenges primarily measure the burden of lead in soft tissues, although whether it accurately reflects long-term exposure or the amount of lead stored in the bone is controversial. Although this technique has been used to determine whether chelation therapy is indicated and to diagnose exposure to heavy metals, some evidence does not support this use as blood levels after chelation is not proportional to the reference range normally used to diagnose heavy metal poisoning. Single chelation doses can also redistribute heavy metals to more sensitive areas such as central nervous system networks.
Epidemiology
Since lead has been used extensively for centuries, the effects of exposure occur worldwide. Leads the environment everywhere, and everyone has multiple levels of measurable blood lead. Atmospheric atmospheric pollution increased dramatically in the 1950s as a result of widespread use of leaded gasoline. Lead is one of the greatest environmental health issues in terms of the number of people exposed and the required public health casualties. Reciprocal exposure accounts for about 0.2% of all deaths and 0.6% years of globally adjusted disability lives.
Although regulation of reduced lead in products has greatly reduced exposure in developed countries since the 1970s, lead is still allowed in products in many developing countries. In all countries that have banned leaded gasoline, the mean blood lead levels have fallen sharply. However, some developing countries still allow leaded gasoline, which is the main source of lead exposure in most developing countries. In addition to gasoline exposure, frequent use of pesticides in developing countries adds to the risk of lead exposure and subsequent poisoning. Poor children in developing countries are at high risk for lead poisoning. Of North American children, 7% have a blood lead level above 10? G/dL, while 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 in Southeast Asia.
In developed countries, people with low levels of education living in poor areas are most at risk for high leads. In the US, the group most at risk of exposure to lead is the poor, urban dwellers, and immigrants. African-American children and those living in old housing are also found to be at high 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, which expose the population to high levels of lead dust.
Risk factors for high lead exposure include alcohol consumption and smoking (probably due to tobacco leaf contamination with lead pesticides). Adults with certain risk factors may be more susceptible to toxicity; these include calcium and iron deficiency, advanced age, lead-targeted organ disease (eg brain, kidney), and possible genetic susceptibility. Differences in susceptibility to lead-induced neurological damage in men and women have also been found, but some studies have found men to be at greater risk, while others have found women to be.
In adults, the level of blood lead continues to increase with age. In adults of all ages, men have higher blood lead levels than women. Children are more sensitive to lead levels in the blood than adults. Children may also have higher tin intake than adults; they breathe faster and may be more likely to have contact with and swallow the soil. Children aged one to three tend to have the highest blood lead levels, perhaps because at that age they begin to walk and explore their surroundings, and they use their mouths in their exploration. Blood levels usually reach about 18-24 months. In many countries including the US, household paint and dust are the main routes of exposure in children.
Important case
Mass lead poisoning cases can occur. 15,000 people were transferred from Jiyuan in central Henan province to another location after 1000 children living around China's largest smelter (owned and operated by Yuguang Gold and Lead) were found to have lead advantages in their blood. The total cost of the project is estimated at about 1 billion yuan ($ 150 million). 70% of the cost will be paid by the local government and the smelter, while the rest will be paid by the residents themselves. The government has stopped production in 32 of 35 tin mills. Affected areas include people from 10 different villages.
Zamfara State led the poisoning epidemic in Nigeria in 2010. On October 5, 2010 at least 400 children have died from the effects of lead poisoning.
Prognosis
Reversal
Results are related to the level and duration of lead exposure. The influence of lead on renal and blood physiology is generally reversible; its impact on the central nervous system is not. While the peripheral effects in adults are often lost when lead exposure stops, evidence suggests that most of the effects of lead on the central nervous system of children can not be altered. Children with lead poisoning may have adverse health, cognitive, and behavioral effects that follow to adulthood.
Encephalopathy
Lead encephalopathy is a medical emergency and causes permanent brain damage in 70-80% of affected children, even those who receive the best care. The mortality rate for people who develop brain involvement is about 25%, and of those with a symptom of encephalopathy when chelation therapy begins, about 40% have permanent neurological problems such as cerebral palsy.
Long-term
Exposure to tin can also reduce age and have long-term health effects. Death rates from a variety of causes have been found to be higher in people with high blood lead levels; These include cancer, stroke, and heart disease, and the general mortality rate of all causes. Lead is considered a human carcinogen that may be based on evidence from animal studies. The evidence also shows that mental decline related to age and psychological symptoms correlates with lead exposure. Cumulative exposure over a prolonged period can have a more important effect on some aspects of health than recent exposure. Some health effects, such as high blood pressure, are only a significant risk when long tin exposure (more than one year).
History
Lead poisoning is one of the best known and most studied occupations and environmental hazards. One of the first metals to be melted and used, lead was thought to have been discovered and was first mined in Anatolia around 6500 BC. Density, workability, and corrosion resistance among metal attractions.
In the 2nd century BC, the Greek botanist, Nicander described colic and paralysis seen in people who are lead poisoning. Dioscorides, a Greek physician who lived in the 1st century, writes that leading makes the mind "give way".
Lead was used extensively in Roman waterways from about 500 BC to 300 AD engineer Julius Caesar, Vitruvius, reported, "water is much healthier than a pottery pipe than from a tin pipe." For that it seems to be made wound by lead, because the white lead is produced by it , and this is said to be harmful to the human body. "Gout, prevalent in prosperous Rome, is considered the result of lead, or leads to the eating and drinking of vessels. Lead sugar (lead (II) acetate) is used to sweeten grapes, and the uric acid produced from this is known as "saturnine" gout. It is even hypothesized that lead poisoning may have caused the decline of the Roman Empire, a completely disputed hypothesis:
The big losses of lead are always toxic. It is fully recognized by the ancients, and Vitruvius specifically warned against its use. Because it was used to produce drinking water, the conclusion was that the Romans had to suffer lead poisoning; sometimes conclusions are made further and it is concluded that this causes infertility and other undesirable conditions, and which causes the pipeline to be largely responsible for the decline and fall of Rome.
Two things that make this interesting hypothesis impossible. First, the precipitated calcium carbonate deposits so thick inside the drains also form inside the pipe, effectively isolating the water from the tin, so they are never touched. Secondly, because the Romans had only a few taps and the water kept flowing, it had not been in the pipeline for more than a few minutes, and certainly not long enough to be contaminated.
However, recent research supports the idea that lead found in water comes from supply pipes, not other sources of contamination. It is not known locals to make holes in the pipes to attract water, increasing the number of people affected by lead.
Thirty years ago Jerome Nriagu argued in a milestone that Roman civilization collapsed as a result of lead poisoning. Clair Patterson, a scientist who convinced the government to ban tin from gasoline, enthusiastically supported the idea, sparking a series of publications aimed at refuting it. Although today's lead is no longer seen as the main cause of Rome's death, its status in water distribution systems with tin pipes (fistulÃÆ'Â|) still stands as a major public health issue. By measuring the composition of the Pb isotope from sediments from the Tiber and Trajanic Ports, this work shows that the "tap water" of ancient Rome has 100 times more water than the spring water.
The Romans also consume tin through the consumption of defrutum, carenum, and sapa, which must be made by boiling the fruit in the lead cooking utensil. Defrutum and his relatives are used in ancient Roman cuisine and cosmetics, including as food preservatives. The use of lead cooking utensils, although popular, is not a common standard and copper cookware is used much more generally. Nor is there any indication of how often greetings are added or in what quantities.
Sapa consumption has a role in the fall of the Roman Empire used in the theory put forward by geochemist Jerome Nriagu to state that "lead poisoning contributed to the decline of the Roman Empire". In 1984, John Scarborough, a pharmacologist and classical, criticized the conclusions drawn by Nriagu's book as "so full of false evidence, mistakes, typographic errors, and flippancy outspoken about primary sources that the reader can not trust the basic argument. "
After ancient times, the mention of lead poisoning did not exist in the medical literature until the late Middle Ages. In 1656, German physician Samuel Stockhausen acknowledged dust and smoke that contained lead compounds as the cause of the disease, dating back to ancient Roman times, the morbi metallici, known to harass the miners, the smelter, the pottery, and others whose work exposing them to metal.
The Caravaggio painter probably died of lead poisoning. A bone with a high lead level was recently discovered in the grave thought that might belong to him. The paint used at the time contains a large amount of lead salt. Caravaggio is known to have exhibited violent behavior, a symptom commonly associated with lead poisoning.
In 17th century Germany, physician Eberhard Gockel discovered tin contaminated wine to be the cause of the colic epidemic. He had noticed that the monks who did not drink healthy wine, while wine drinkers developed colic, and traced the cause to tin sugar, made by boiling litharge with vinegar. As a result, Eberhard Ludwig, Duke of WÃÆ'¼rttemberg issued a decree in 1696 banning wine counterfeiting by litharge.
In the 18th century lead poisoning was quite frequent because of the large amount of rum drinking, which was made silent by the main component ("worms"). It was a significant cause of death among slaves and sailors in the colonial West Indies. Lead poisoning from rum is also recorded in Boston. Benjamin Franklin allegedly caused the risk in 1786. Also in the 18th century, "Devonshire colic" was the name given to the symptoms suffered by Devonians who drank the essence made with a pressed press. Lead added to illegally cheap wine in the 18th and early 19th century as a sweetener. Beethoven composer, a heavy wine drinker, suffers from an increase in lead levels (as detected in his hair) probably because of this; the cause of death is controversial, but lead poisoning is a competitor as a factor.
With the Industrial Revolution of the 19th century, lead poisoning became common in the workplace. The introduction of lead paint for the use of housing in the 19th century increased the exposure of childhood to leadership; For thousands of years before this, most of the lead exposure was work. An important step in the understanding of lead poisoning in childhood occurred when the toxicity of children from lead paint was recognized in Australia in 1897. France, Belgium and Austria banned white lead paint in 1909; The League of Nations followed him in 1922. However, in the United States, a law that prohibited primary house paint was not ratified until 1971, and was phased out and not completely banned until 1978.
The 20th century experienced an increase in the level of lead exposure around the world due to the increasing use of the metal widely. Start
Source of the article : Wikipedia
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