Lead poisoning

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aksiniya Stevasarova, M.D. Leena Josephin Jetty, M.B.B.S[2]

Lead poisoning is a medical condition, also known as saturnism, plumbism, or painter’s colic caused by increased blood lead levels. Lead may cause irreversible neurological damage as well as renal disease, cardiovascular effects, and reproductive toxicity.

Humans have been mining and using this heavy metal for thousands of years, poisoning themselves in the process due to accumulation and exposure. These dangers have long been known, though the modern understanding of their full extent and the small amount of lead necessary to produce them is relatively recent; blood lead levels once considered safe are now considered hazardous, with no known threshold. Reducing these hazards requires both individual actions and public policy regulations. ^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aksiniya Stevasarova, M.D. Leena Josephin Jetty, M.B.B.S[2]

Lead toxicity was first recognized as early as 200 BC.

• Nicander of Colophon wrote of lead-induced anemia and colic in 250 BC.^[1] Gout, prevalent in affluent Rome, is thought to be the result of lead, or leaded eating and drinking vessels. Lead was used in makeup. Sugar of lead (lead(II) acetate) was used to sweeten wine, and the gout that resulted from this was known as saturnine gout. ^[2]

• The symptoms of Lead Poisoning were described in the book De Materia Medica ,the leading pharmacological text for centuries written by Dioscorides. ^[3]

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

• There have been several outbreaks of [disease name], which are summarized below:
• Though Lead was known to exist for thousands of years its use surged in the 20 th century as it was found to reduce burning of fuel and decrease the “engine Knock”,due to its malleable nature it was used for transporting drinking water, soldering food cans, making paints durable and bright, and killing insects. About 80% of workers in Standard oil NJ ,manufacturing tetraethyl lead were found to have lead poisoning .The discovery of which lead to the ban of leaded gasoline in NY and NJ^[4]

• In [year], [diagnostic test/therapy] was developed by [scientist] to treat/diagnose [disease name].

• Aulus Cornelius Celsus, writing ca. 30 AD, listed white lead on a list of poisons with antidotes (beside cantharides, hemlock, hyoscyamus, poisoned mushrooms, and a swallowed leech), and claimed it could be remedied by mallow or walnut juice rubbed up in wine.

^{[5] [6] [7]}

• Despite his awareness of lead’s toxicity, citing many contemporary authorities, Celsus recommended its use in a wide range of ointments applied to wounds to stop bleeding and reduce infection or inflammation. ^[8]

• Lead poisoning, was rather frequent in the 18th century, due to the widespread drinking of rum, which was made in stills with a lead component (the “worm”). It caused the death of many slaves and sailors in the colonial West Indies. Lead poisoning due to rum consumation was also observed in in Boston. 

• In 1786 Benjamin Franklin suspected that lead might be toxic.

• Also in the 18th century, the abdominal pain that people of Devon, who drank cider made in presses lined with lead, was referred to as “Devonshire colic”. ^[9]
• In the 18th and early 19th centuries, lead was even added to cheap wine as a sweetener. One of the most famous composers of all times, Ludwig van Beethoven, who lived during this time period and who was also a heavy wine drinker, suffered elevated lead levels (as later detected in his hair) possibly due to that reason. The cause of his death is still arguable, but lead poisoning is definitely one of the possible causes.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aksiniya Stevasarova, M.D.

Lead poisoning or Lead intoxication is defined as exposure to high levels of lead associated with clinical symptoms.^[1]. Poisoning is defined as symptoms that occur with toxic effects from high levels of exposure; Toxicity is a wider spectrum of effects, including the subclinical ones-that do not cause symptoms.^[2] However, we 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.^[2]

• There is no established system for the classification of lead poisoning.

• Based on the amount of lead in the blood and tissues, as well as the time of exposure, lead poisoning may be classified as either 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.^[3]

• Lead forms a variety of compounds and exists in the environment in various forms.^[4] 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 ceased to use 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.^[5]

• 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). Urine lead levels may be used as well, though less commonly. In cases of chronic exposure lead often sequesters in the highest concentrations first in the bones, then in the kidneys. ^[6]

• 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.>^[7] Authorities such as the American Academy of Pediatrics define lead poisoning as blood lead levels higher than 10 μg/dL.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aksiniya Stevasarova, M.D. Leena Josephin Jetty, M.B.B.S[2]

Lead poisoning is a medical condition, also known as saturnism, plumbism, or painter’s colic caused by increased blood lead levels. Lead may cause irreversible neurological damage as well as renal disease, cardiovascular effects, and reproductive toxicity. Humans have been mining and using this heavy metal for thousands of years, poisoning themselves in the process due to accumulation and exposure. These dangers have long been known, though the modern understanding of their full extent and the small amount of lead necessary to produce them is relatively recent; blood lead levels once considered safe are now considered hazardous, with no known threshold. Reducing these hazards requires both individual actions and public policy regulations. ^[1]

• Lead has no known physiologically relevant role in the body.
• Lead a divalent metal similar to calcium, iron and zinc uses channels like calcium channel or Divalent Metal Transporter(DMT) and enters the cells and acts as a cofactor to enzymes.^[2]
• Once Lead is absorbed it gets deposited in the bones(70% in adults and 95% in children).
• Roughly 1% circulates in the blood,99% of which is in the RBC’s.^[3]
• The toxicity of lead comes from its ability to mimic other biologically important metals, most notably calcium, iron and zinc which act as cofactors in many enzymatic reactions.
• Following ingestion, lead is able to bind to and interact with many of the same enzymes as these are metals, but due to its differing chemistry, does not properly function as a co-factor, thus interfering with the enzyme’s ability to catalyze its normal reaction(s).
• Lead toxicity symptoms arise are thought to occur by interfering with an essential enzyme delta-AminoLevulinic Acid Dehydratase, or ALAD. ALAD is a zinc-binding protein which is important in the biosynthesis of heme, the co-factor found in hemoglobin. Lead poisoning also inhibits the enzyme ferrochelatase which catalyzes the joining of protoporphyrin IX and Fe2+ to form Heme. ^{[4] [5]}

File:Sources of lead poisoning and its effects(1).jpg

• Lead exposure in childhood is associated with decreased brain volume; this might be due to reduced neuronal size/dendritic arborisation and this reduced volume of brain persists into adulthood.^[6]

• Lead exposure is a known risk factor for Chronic Kidney Disease(CKD)^[7]
• Nephrotoxic effects include
• Intra nuclear inclusion bodies in Proximal Tubule cells
• Tubulo interstitial fibrosis
• It can cause decrease in Glomerular Filtration Rate(GFR).

• Lead causes cellular changes that are characteristic for hypertension and atherosclerosis.
• Laboratory studies revealed that chronic ,Low level lead exposure increases oxidative stress, decreases nitric oxide levels and induces vast spasm by activating protein kinase C there by causing hypertension.
• By inactivation of nitric oxide, increased hydrogen peroxide levels, inhibition of endothelial repair, impairing angiogenesis, promoting thrombus formation causes atherosclerosis.^[8]

• So far three polymorphic genes have been identified to be able to potentially influence the bioaccumulation and toxicokinetics of lead in humans. These genes are delta-aminolevulinic acid dehydratase (ALAD) gene, the hemochromatosis gene and the vitamin D receptor (VDR). Their relation to susceptibility especially to lead nephrotoxicity in high lead-exposed workers has been established. ^{[9] [10]}

• Delta -aminolevulinic acid dehydratase (ALAD) plays an important role in lead poisoning, and polymorphisms in the ALAD gene might affect the symptoms the individual patients experience. ^[11]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aksiniya Stevasarova, M.D.

Common causes of lead poisoning include ingestion, inhalation and skin exposure to lead and lead particles.

• Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.
• Life-threatening causes of lead poisoning include ingestion of lead base paint by small children, eventually leading to seizures, unconsciousness, coma and even death.

Lead poisoning may be caused by:

• Occupational hazards
  • 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, fetal monitors, plumbing, circuit boards, jet engines, and ceramic glazes, 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.^{[1] [2] [2] [3]}

• Ingestion of lead contaminated soil
  • Tetraethyllead, which used to be added to automotive gasoline (and still is added to some aviation gasolines), contributed to soil contamination. Residual lead in soil contributes to lead exposure in urban areas.^[4]

• Ingestion of lead dust or chips from deteriorating lead-based paints.
  • Lead compounds are very colorful and are used widely in paints, ^[5] and lead paint is a major route of lead exposure in children.^[6] A study conducted in 1998–2000 found that 38 million housing units in the US had lead-based paint, down from a 1990 estimate of 64 million.^[7] Deteriorating lead paint can produce dangerous lead levels in household dust and soil.^[8] Deteriorating lead paint and lead-containing household dust are the main causes of chronic lead poisoning.^[9] The lead breaks down into the dust and since children are more prone to crawling on the floor, it is easily ingested.^[7]

• Drinking tap water.
  • It can come from plumbing and fixtures that are either made of lead or have trace amounts of lead in them.^{[10] [11][12]}

Less common causes of lead poisoning include exposure to metallic lead via:

• • Imported cosmetics such as Kohl and Surma
  • Folk remedies like Azarcon which contains 95 percent lead and is used to “cure” empacho.
  • Contracted through the mucous membranes through direct contact to mouth, nose, eyes, and breaks in skin.

• Lead poisoning is not caused by a mutation in any gene.
• On the other hand so far three polymorphic genes have been identified to be able to potentially influence the bioaccumulation and toxicokinetics of lead in humans. These genes are delta-aminolevulinic acid dehydratase (ALAD) gene, the hemochromatosis gene and the vitamin D receptor (VDR). Their relation to susceptibility especially to lead nephrotoxicity in high lead-exposed workers has been established. ^{[13] [14]}
• Delta -aminolevulinic acid dehydratase (ALAD) plays an important role in lead poisoning, and polymorphisms in the ALAD gene might affect the symptoms the individual patients experience. ^[15]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aksiniya Stevasarova, M.D.

Lead poisoning must be differentiated from megaloblastic anemia^[1], carpal tunnel syndrome^[2], Guillain–Barré syndrome, renal colic, appendicitis, encephalitis in adults, and viral gastroenteritis in children.^[3], constipation, abdominal colic^[4], iron deficiency, subdural hematoma, neoplasms of the central nervous system, emotional and behavior disorders, and intellectual disability.^{[5] [6]}

• As lead poisoning manifests in a variety of clinical forms, differentiation must be established in accordance with the particular clinical symptom. ^[7]
  • Sideroblastic anemia must be differentiated from other diseases that cause basophilic stippling like megaloblastic anemia^[1].
  • Peripheral neuropathy must be differentiated from Guillain–Barré syndrome, which will present with albuminocytological dissociation on CSF analysis.
  • Intellectual disability must be differentiated from autism, Down syndrome, Fragile X syndrome
  • Abdominal colic must be differentiated from Gallbladder disease, viral gastroenteritis, pancreatitis etc.^[4]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aksiniya Stevasarova, M.D.

Lead constitutes 0.002% of the Earth’s crust, and in nature it exists mainly as lead sulphide. Lead has become widely distributed in the biosphere only in the past few thousand years, almost entirely as the result of human activity (National Research Council, 1972). Once lead is introduced into the environment, it persists. The average person has less than 10 micrograms per deciliter, or 100 parts per billion, ppb, of lead in their blood. People who have been exposed to an unusual amount of lead will have blood lead levels higher than 200 ppb—most clinical symptoms of lead poisoning begin at around 100 ppb. The effect on children’s mental/cognitive abilities has been noted at very low levels.^[1]

• The incidence of lead poisoning is approximately one in 38 U.S. children in the United States.
• Low income people often live in rental housing with lead paint, and unless the landlord conducts regular inspections, paint may begin to peel and residents will be exposed to high levels of lead paint dust, thus greatly increasing their chance of lead poisoning.

• The prevalence of lead poisoning in children, according to the CDC, in the United States is estimated to be approximately half million children ages 1-5 with blood lead levels above 5 micrograms per deciliter (µg/dL). The percentage of children in the same age group with blood lead levels greater than or equal to 10 µg/dl has declined from 77.8% in the late 1970s to 4.4% in the early 1990s, and the average lead level of a child in the United States has declined to 1.9 µg/dl between 1999 and 2002.
• Today at least 4 million households have children living in them that are being exposed to high levels of lead.
• In 1978 there were 13.5 million children in the United States with elevated blood lead levels (i.e., 10µg/dl). By 2002, that number had dropped to 310,000 children.^[2] The U.S. incurs $43.4 billion annually in the costs of all pediatric environmental disease, with childhood lead poisoning alone accounting for the vast majority of it.^[3]

• The case-fatality rate of lead poisoning is approximately 400,000 U.S. deaths per year.

• Patients of all age groups may develop [[lead poisoning].
• The incidence of lead poisoning is higher in children; the median age at diagnosis is 1-5 years.
• Lead poisoning commonly affects individuals younger than 10 years of age.
• Chronic lead poisoning is usually first diagnosed adults.
• Acute lead poisoning commonly affects children.

• Children

Lead-contaminated household dust is the major source of lead exposure to children in the U.S.^[4] A 2006 study in New York City found lead levels in settled outdoor dust, which is a source of household dust, of 175 to 730 μg/ft², and noted that these levels exceed the HUD/EPA lead in indoor dust standard of 40 μg/ft².^[5]

• Adults

Although children are at greater risk from lead exposure, adult exposures can also result in harmful health effects. Most adult exposures are occupational and occur in lead-related industries such as lead smelting, refining, and manufacturing industries. One frequent source of lead exposure to adults is home renovation that involves scraping, remodeling, or otherwise disturbing lead-based paint. Adults can also be exposed during certain hobbies and activities where lead is used. Workers may inhale lead dust and lead oxide fumes, as well as eat, drink, and smoke in or near contaminated areas, thereby increasing their probability of lead ingestion. Between 0.5 and 1.5 million US workers are exposed to lead in the workplace (ATSDR, 1999). Other than the developmental effects unique to young children, the health effects experienced by adults from adult exposures are similar to those experienced by children, although the thresholds are generally higher.^[6]

• There is no racial predilection to lead poisoning.
• Lead poisoning usually affects many people through household products, workplace, and lead paint, studies show that people of color and recent immigrants are at a much greater risk for high levels of exposure than whites ^[7].

• Lead poisoning affects men and women equally.

• The majority of lead poisoning cases are reported in the developing countries.

• According to the CDC and WHO in the United States, the phasing-out of leaded petrol between 1976 and 1995 was associated with a more than 90% reduction in mean blood lead concentration. Similar effects were recorded in western Europe, Australia, Canada, New Zealand and South Africa (von Schirnding & Fuggle, 1996; Landrigan, 2002). In a number of rapidly industrializing countries, too, including China, El Salvador, India, Mexico and Thailand, declines in blood lead levels have followed the removal of lead from petrol (OECD, 1999; Mathee et al., 2006; He, Wang & Zhang, 2009). Worldwide, unleaded petrol now accounts for an estimated 99% of total sales. T

• According to the CDC and WHO by the late 2010, almost all countries have phased out leaded petrol, leaving 9 countries with leaded petrol. Three countries are using only leaded petrol (North Korea, Myanmar, Afganistan), and 6 countries (Algeria, Iraq, Montenegro, Serbia, Yemen, Bosnia-Herzegovina) are using both leaded and unleaded petrol.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aksiniya Stevasarova, M.D.

Today almost everyone is exposed to environmental lead. The most potent risk factors in the development of lead poisoning are trough inhalation, ingestion or occasionally dermal contact with lead or lead particles.

• Common risk factors in the development of lead poisoning include:
  • Lead mining and lead smelting, where children and adults can receive substantial lead exposure from sources uncommon today in the U.S.
  • ingestion of lead particles is common risk factor in the development of lead poisoning in children in the United States.
  • Inhalation is the second major pathway of exposure. Inhalation also contributes to lead body burden and may be the major contributor for workers in lead-related occupations. Almost all inhaled lead is absorbed into the body, whereas from 20% to 70% of ingested lead is absorbed (with children generally absorbing a higher percentage than adults do).
  • Dermal exposure plays a role for exposure to organic lead among workers, but is not considered a significant pathway for the general population, except in areas where leaded gasoline is used. Organic lead from gasoline additives may be absorbed directly through the skin.^[1]
  • Soil represents another major risk factor for lead poisoning. Tetraethyllead, which used to be added to automotive gasoline (and still is added to some aviation gasolines), contributed to soil contamination. Residual lead in soil contributes to lead exposure in urban areas.^[2] 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;^[3] eating food grown in contaminated soil can present a lead hazard.^[4]
  • Lead from the atmosphere or soil can end up in groundwater and surface water.^[5] It is also potentially in drinking water, e.g. from plumbing and fixtures that are either made of lead or have lead solder.^[6][7] 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.^[6] Chloramines, which were adopted as a substitute for chlorine disinfectants due to fewer health concerns, increase corrositivity.^[8] In the US, 14–20% of total lead exposure is attributed to drinking water.^[8] 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.^[9][10] In the Flint water crisis, a switch to a more corrosive municipal water source elevated lead levels in drinking water in domestic tap water.^[11][12]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aksiniya Stevasarova, M.D.

According to the CDC, screening for [lead poisoning] by blood lead test is recommended every for children aged 6 up to 36 and 36 to 72 months.“CDC – Childhood Lead Poisoning Prevention Program – PLPYC 91 Chapter 6”.

According to the CDC, screening for [lead poisoning] by blood lead test is recommended for virtually all children. Screening children with high probability of exposure to high-dose sources is the highest priority. Children at greatest risk for high-dose lead exposure should be screened more frequently. “CDC – Childhood Lead Poisoning Prevention Program – PLPYC 91 Chapter 6”.

According to the CDC, children ages 6 to 72 months who live in or are frequent visitors to deteriorated old buildings, including day care centers, make up the highest priority group. Because the highest concentrations of lead in paint were used in the early 1900s, homes built before about 1960 are of greatest concern. Children whose homes are being renovated are also at extremely high risk. Because almost all U.S. children are at risk for lead poisoning (although some children are at higher risk than others), our goal is that all children should be screened, unless it can be shown that the community in which these children live does not have a childhood lead poisoning problem. “CDC – Childhood Lead Poisoning Prevention Program – PLPYC 91 Chapter 6”.

Screening Schedule

• Children 6 up to 36 months of age:
  • A child at low risk for exposure to high-dose lead sources by questionnaire should have an initial blood lead test at 12 months of age.

If the 12-month blood lead result is < 10 µg/dL, the child should be retested at 24 months if possible, since that is when blood lead levels peak. If a blood lead test result is 10-14 µg/dL, the child should be retested every 3 to 4 months. After 2 consecutive measurements are < 10 µg/dL or three are < 15 µg/dL, the child should be retested in a year.“CDC – Childhood Lead Poisoning Prevention Program – PLPYC 91 Chapter 6”. If any blood lead test result is > or = to 15 µg/dL, the child needs individual case management, which includes retesting the child at least every 3 to 4 months.

• • A child at high risk for exposure to high-dose lead sources by questionnaire should have an initial blood lead test at 6 months of age.

If the initial blood lead result is < 10 µg/dL, the child should be rescreened every 6 months. After 2 subsequent consecutive measurements are < 10 µg/dL or three are < 15 µg/dL, testing frequency can be decreased to once a year.“CDC – Childhood Lead Poisoning Prevention Program – PLPYC 91 Chapter 6”. If a blood lead test result is 10-14 µg/dL, the child should be screened every 3 to 4 months. Once 2 subsequent consecutive measurements are < 10 µg/dL or three are < 15 µg/dL, testing frequency can be decreased to once a year. If any blood lead test result is > or = to 15 µg/dL, the child needs individual case management, which includes retesting the child at least every 3 to 4 months.“CDC – Childhood Lead Poisoning Prevention Program – PLPYC 91 Chapter 6”.

• Children > or = to 36 months and less than 72 months age:
  • All children who have had venous blood lead tests > or = to 15 µg/dL or who are at high risk by questionnaire should be screened at least once a year until their sixth birthday (age 72 months) or later, if indicated (for example, a developmentally delayed child with pica). “CDC – Childhood Lead Poisoning Prevention Program – PLPYC 91 Chapter 6”.
  • If the blood lead level is 15-19 µg/dL, the child should be screened every 3-4 months, the family should be given education and nutritional counseling as described in Chapter 4, and a detailed environmental history should be taken to identify any obvious sources or pathways of lead exposure. When the venous blood lead level is in this range in two consecutive tests 3-4 months apart, environmental investigation and abatement should be conducted, if resources permit.“CDC – Childhood Lead Poisoning Prevention Program – PLPYC 91 Chapter 6”.
  • If the blood lead level is > or = to 20 µg/dL, the child should be given a repeat test for confirmation. If the venous blood lead level is confirmed to be > or = to 20 µg/dL, the child should be referred for medical evaluation and followup. Such children should continue to receive blood lead tests every 3-4 months or more often if indicated. Children with blood lead levels > or = to 45 µg/dL must receive urgent medical and environmental followup, preferably at a clinic with a staff experienced in dealing with this disease. Symptomatic lead poisoning or a venous blood lead concentration > or = to 70 µg/dL is a medical emergency, requiring immediate inpatient chelation therapy.“CDC – Childhood Lead Poisoning Prevention Program – PLPYC 91 Chapter 6”.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aksiniya Stevasarova, M.D.. Leena Josephin Jetty, M.B.B.S[2]

If left untreated, 100% of patients with [lead poisoning] may progress to develop seizures, unconsciousness and death.

• Symptoms of acute lead poisoning usually develop in the first 3 year of life, and start with symptoms such as pain, muscle weakness, numbness and tingling, and, rarely, symptoms associated with encephalitis.^[1] Abdominal pain, nausea, vomiting, diarrhea, and constipation are other acute symptoms.^[2] Lead’s effects on the mouth include astringency and a metallic taste.^[2] 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 circulatoryshock due to loss of water from the gastrointestinal tract.^[2] Hemolysis due to acute poisoning can cause anemia and hemoglobinuria.^[2] Damage to kidneys can cause changes in urination such as oliguria.^[2]

• Common complications of lead poisoning include:
  • gastrointestinal
  • neuromuscular
  • neurological

Central nervous system and neuromuscular symptoms usually result from intense exposure, while gastrointestinal symptoms usually result from exposure over longer periods.^[2] 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.^[3] Fatigue, problems with sleep, headaches, stupor, slurred speech, and anemia are also found in chronic lead poisoning.^[1] A “lead hue” of the skin with pallor and/or lividity is another feature of chronic lead poisoning.^[4][5] A blue line along the gum with bluish black edging to the teeth, known as a Burton line, is another indication of chronic lead poisoning.^[6] Children with chronic poisoning may refuse to play or may have hyperkinetic or aggressive behavior disorders.^[1] Visual disturbance may present with gradually progressing blurred vision as a result of central scotoma, caused by toxic optic neuritis.^[7]

• Studies conducted in the recent past have confirmed that long term exposure of low levels of lead, which were previously determined to be safe are a major risk factor for atherosclerotic cardiovascular disease in adults and cognitive deficits in children. The effects of exposure to lead on long term basis varies in children and adults.

Complications

• Low level lead poisoning in children was found to be a risk factor for :
  • Preterm Labor
  • Cognitive defects
  • Attention Deficit Hyperkinetic Disorder(ADHD)
  • Elevated Blood Pressure
  • Reduced Heart rate variability.
• In adults it is associated with :
  • CKD
  • Hypertension

• Lead exposure is found to be a risk factor for preterm birth ,a 10 microgram elevation in blood lead levels is associated with 70 % increase in preterm birth.For those with Vitamin D deficiency this risk is even more elevated.
• Lead exposure is associated with reduced I.Q ,with higher reductions occurring at relatively low levels of exposure.^[8]
• Childhood exposure to Lead is a known risk factor for anti social disorders ,including
  • Conduct disorder
  • Delinquent behaviour
  • Criminal behaviour.

• • In Adults:
• Higher blood or bone levels are found to be congruently associated with accelerated cognitive decline; especially in those withAPOE4 alleles, drawing suspicion that it may have a role as a risk factor for late onset Alzheimer’s disease.

• Lead causes cellular changes that are characteristic for hypertension and atherosclerosis.Is is a leading risk factor for death from cardiovascular disease. *Laboratory studies revealed endothelial cells incubated in lead for 72 hours at concentrations of 0.14 to 8.2 μg per liter showed signs of membrane damage , which is the earliest finding in the natural history of atherosclerosis.
• Studies revealed that the risk of death from cardiovascular disease and coronary artery disease increased sharply at levels below 50 μg per liter, when adjusted for other risk factors.

• The incidence of hypertension in the U.S decreased tremendously during the phaseout of leaded gasoline.
• The usual factors like smoking, antihypertensive medicines, obesity, or even the larger size of the cuff used to measure blood pressure in persons with obesity — did not explain the decline.but it was observed that the median blood lead levels dropped by 100 μg per litre over a period of 18 years, which point towards the role of Lead in the causation of hypertension^[9]

• Lead causes cellular changes that are characteristic for hypertension and atherosclerosis.Is is a leading risk factor for death from cardiovascular disease. *Laboratory studies revealed endothelial cells incubated in lead for 72 hours at concentrations of 0.14 to 8.2 μg per liter showed signs of membrane damage , which is the earliest finding in the natural history of atherosclerosis.
• Studies revealed that the risk of death from cardiovascular disease and coronary artery disease increased sharply at levels below 50 μg per liter, when adjusted for other risk factors.

• The incidence of hypertension in the U.S decreased tremendously during the phaseout of leaded gasoline.
• The usual factors like smoking, antihypertensive medicines, obesity, or even the larger size of the cuff used to measure blood pressure in persons with obesity — did not explain the decline.but it was observed that the median blood lead levels dropped by 100 μg per litre over a period of 18 years, which point towards the role of Lead in the causation of hypertension^[9]

• Prognosis is generally related to the extent and duration of lead exposure.^[10]

Effects of lead on the physiology of the kidneys and blood are generally reversible; its effects on the central nervous system are not.^[11] 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.^[12] Children with lead poisoning may thus have adverse health, cognitive, and behavioral effects that follow them into adulthood.^[13]

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