Lead is estimated to be responsible for 900,000 deaths globally and 21,000 deaths in the US, with nearly 75% of these deaths due to cardiovascular disease.
Lead exposures have declined in high income countries, but remain high globally as a result of the rising demand for lead batteries and continued use of lead paint.
Withfew exceptions, such as aviation fuel and ammunition, and lead acid batteries for motor vehicles, lead is no longer used in the US and Europe.
Lead is a heavy metal in the earth that is released into the environment primarily through human extraction and processing.
Exposures linger from lead paint in older houses, deposition of leaded gasoline in the soil, leaching of lead from water lines, and the emissions from industrial plants and incinerators.
Lead is typically absorbed through inhalation or ingestion.
Almost 99% of absorbed lead binds to erythrocytes.
Lead is deposited in tissues such as the kidney, brain, or liver, and it is ultimately sequestered in bones, where its half life ranges from 20 to 30 years.
Low level of lead poisoning is a risk factor for cardiovascular disease in adults and congenital deficits in children.
In 2019 an estimated 5.5 million deaths from cardiovascular disease were attributed to lead exposure.
Lead exposure is a leading factor for the risk of death from cardiovascular disease.
Low level poisoning is a risk factor for preterm birth, and for cognitive deficits and attention deficit hyperactivity disorder as well as hypertension and heart rate variability in children.
Studies suggest 250,000 premature deaths from cardiovascular disease each year are due to chronic, low level lead poisoning.
Dropping levels of coronary heart disease have been partially attributed to decreased exposure to lead in recent decades.
Children with higher levels of lead dentin are more likely to have neuropsychological deficits and have unfavorable ratings on distractibility, organizational ability, impulsivity, and other behavioral characteristics and children with lower dentin lead levels.
Lead level exposures is a risk factor for behavioral conditions such as ADHD.
Childhood lead exposure is related to antisocial behaviors, including conduct disorders, delinquent behavior, and criminal behavior.
Higher childhood lead exposure is associated with deductions in brain volume, and the reduced volume persists into adulthood.
In adulthood higher blood or bone lead levels are associated with cognitive decline, particularly an individuals with APOE4 alleles.
In adults low level lead poisoning as a risk factor for chronic kidney failure, hypertension, and cardiovascular disease.
Poisoning occurs both in children and adults.
The diagnosis of lead poisoning is often overlooked.
lead is readily absorbed by rapidly growing infants.
Lead absorption can be enhanced in the context of iron or calcium deficiency.
Lead, mimicking, calcium, iron, and zinc can enter cells through calcium channels and metal transporters.
Lead absorption is increased with certain genetic polymorphisms, which can enhance iron or calcium absorption, such as those that cause hemochromatosis.
Ubiquitous in the environment that has no known biological role in humans.
Ingestion, and inhalation are the primary routes of lead exposure.
95% of lead absorbed is retained in adult skeletons and in children 70% is stored in the skeleton.
One percent of the total body lead burden is circulating in blood, while 99% of lead in blood is found in red blood cells.
Hyperthyroidism and menopause release lead sequestered in the skeleton, increasing blood lead concentrations.
Toddlers who live in poorly maintained housing built before 1960 are at risk for life poisoning from ingestion of paint chips and lead contaminated house dust.
People who drink tapwater from lead service lines or live near airports or other sites that emit lead pollution have increased risk for low level lead poisoning.
Airborne lead concentrations are markedly higher in racially segregated communities.
Workers in smelting, battery recycling, and construction, as well as persons who are use firearms, or have retained bullet fragments in their bodies are at increased risk for lead poisoning.
Lead is a known risk factor for hypertension.
Can form complexes with amino acids, proteins, and thiol-containing compounds, resulting in inhibition of enzymes and induction of oxidative stress.
Exposure can result in acute or chronic adverse effects and multiple organ systems, ranging from subclinical life-threatening processes.
Acute and chronic lead poisoning cad lead to long-term health benefits including: irreversible cognitive and renal impairment, increased risk of hypertension and cardiac death.
Mild elevation of blood lead levels are typically asymptomatic, but are associated with long-term toxic affects.
There is decreasing blood levels in the US population over the years.
Blood levels in the adult population have declined to a current average of 0.92 µg per deciliter.
For adults the elevated blood level for lead in adults is 5 µg per dL.
There is no safe blood level established.
To prevent adverse health effects of blood levels in adults should be less than 10 µg/dL.
In adults can cause toxicity to the bone marrow, liver, kidneys, and CNS.
It is a multisystem toxicant with dose related effects on the blood, brain, cardiovascular, renal, and reproductive systems.
Clinical effects of lead depend on the quantity and duration of lead exposure.
Acute and subacute lead poisoning frequently cause abdominal pain, fatigue, neurologic symptoms such as irritability and headache, and anemia.
Severe acute lead poisoning can result in encephalopathy and death.
Severe acute lead poisoning can result in encephalopathy and death.
Chronic exposure is more common then acute exposure, and is often subclinical with many adverse health consequences:neurodevelopmental delay in children and cardiovascular disease in adults.
Studies have shown lead exposure leads to progressive decline in IQ, and such a decline is a risk factor for degenerative brain diseases, including dementia.
In a longitudinal cohort study of a median 34 years of follow up, higher childhood blood levels were associated with differences in some MRI measures of brain structure suggesting lower structural brain integrity in mid life. (Ruuben, Aaron).
High blood levels associated with an increase in systolic blood pressure and mortality.
Anemia associated with lead can be attributed impaired heme synthesis, shortened rbc survival, and impaired renal production of erythropoietin.
With very high lead levels I have a greater than 100 µg per deciliter encephalopathy which can include seizures can occur.
Basophilic stippling is a non-specific findings with lead poisoning.
It interferes with two of the enzymes involved in heme synthesis: delta aminolevulinic acid dehydratase and ferroochelatase.
Colicky abdominal pain can occur in adults with high blood levels that exceed 80 µg perdL, whereas milder nonspecific G.I. discomfort and constipation occur with levels higher than 60 µg per deciliter, and myalgias at levels higher than 40 to 70 µg per deciliter.
Typical presentation includes: abdominal pain, weight loss, and microscopic anemia.
Children have exposure to chewing on objects with lead based paint.
Many of the adverse health effects of lead exposure are irreversible.
Risk factors for lead exposure include socioeconomic factors of the lower family income, older housing, poor nutritional status, living near industries that involve lead, proximity to renovation or deterioration of older homes with lead based paint, and previously living in countries will lead exposure is high.
Adults working in battery factories or lumbers exposed to inhaled lead dust can lead to lead poisoning.
Pregnant women with high blood lead levels are at risk of spontaneous abortion.
Lead exposure is it a risk factor for preterm births at concentrations commonly found in pregnant women.
In a Canadian study an increase of 10 µg per liter in the maternal blood level was associated with the 70% increase in the risk of spontaneous preterm birth.
In pregnant women, lead exposure can impair organ systems such as the hematopoetic, hepatic, renal, and nervous systems and increase the risk of preeclampsia and adverse perinatal outcomes.
Elevated blood levels in children are associated with neurological effects such as behavioral and learning problems, lower IQ, hyperactivity, hearing problems, and impaired growth.
Children are at the highest risk for lead poisoning and high blood levels are associated with reduced intelligence, ADHD, hearing impairment, and delayed puberty in girls.
Lead added to house paint increases durability and resists moisture, but has been banned since 1978 from indoor house painting.
Approximately 95% of all elevated blood lead levels among adults in the United States are work-related.
Analysis 2008-2009 showed a decline in the prevalence of elevated blood lead levels was from 14 per 100,000 employed adults in 1994 to 6.3 in 2009.
A heme synthesis inhibitor.
Better absorbed in the presence of zinc or calcium deficiencies.
Inhibits zinc dependent enzymes.
Replaces calcium in bones and replaces calcium utilized for brain neurotransmitter release.
Inhibits f2242ochelatase in the heme pathway resulting in protoporhyrin IX accumulation.
Inhibits prophobilinogen (PBG) synthetase with accumulation of delta-amminolevulinic acid (ALA)
ALA resembles gamma-amino butyric acid (GABA) and may account for acute lead poison psychosis.
Chronic accumulation results in interstitial nephritis and renal insufficiency.
Children’s exposure can cause impaired intelligence and changes in behavior in the absence of clinically visible symptoms of lead toxicity.
Lead exposure can result irreversible harm in children.
Lead can cross the placenta and elevated lead levels in pregnant women pose risks with respect to pregnancy outcomes of gestational hypertension, spontaneous abortion, fetal developmental delays, reduce IQ and behavior problems.
Lead poisoning has been described in the autism spectrum disorders.
High chronic exposure of greater than 70-80 mcg/deciliter causes chronic kidney disease in adults and children.
Blood levels of lead less than 10 mcg/deciliter may be associated compared kidney function in adults.
Higher blood levels of lead at baseline was prospectively associated with more rapid kidney function decline than lower levels (Yu CC).
The current CDC level for blood lead level concentrations is 5 mcg per deciliter.
Blood lead levels in adults, even below 5 mcg/deciliter have been associated with increased prevalence of chronic kidney disease.
In a study of US adolescents higher blood levels were associated with lower GFR, and this association was throughout the range of lead blood levels, with more than 99% of participants having blood levels below 10 mcg per deciliter (The Third National Health and Nutrition Examination Survey,Fadrowski J).
Acute lead exposure can cause damage to the proximal tubule of the kidney.
Chronic lead exposure leads to interstitial fibrosis in kidney.
Children living near smelters of lead, and adolescents working in auto shops in developing nations have increased urinary biomarkers of kidney dysfunction.
Lead induces cellular alterations characteristic of hypertension and atherosclerosis, increases oxidative stress, reduces levels of biologically, active nitric oxide, and induces vasoconstriction.
The incidence of hypertension has decreased in part related to phaseout of leaded gasoline.
Lead exposure is a leading risk factor for death from coronary heart disease.
Reducing lead exposure results in reductions in blood pressure and the risk of cardiovascular disease within one to two years.
The use of chelation therapy to lower lead levels in a randomized trial of 64 adult patients with chronic kidney disease showed improvement in GFR compared to a control group (Yu CC).
The most common source of exposure for lead poisoned children age 6 years or less in the US is lead based paint, but increasingly exposure to lead an immigrant groups comes from use of imported products such as spices, food, candy, cosmetics, pottery and jewelry.
Childhood blood lead levels are significantly associated with higher general psychopathology and internalizing and thought disorder symptoms in adulthood.
Clinical findings on physical examination consistent with lead poisoning include: bluish pigmentation of the gumline, termed lead lines, hypertension, and peripheral neuropathy.
Childhood blood lead levels are significantly associated with lower conscientiousness and agreeableness and higher neuroticism in adulthood.
Lead exposure has decreased substantially in the United States related to phaseout of residential lead-based paints in 1978, lead gasoline phased out and band by 1996.
Exposure to lead most commonly occurs to occupational exposure is associated with the removal of old paint, demolition of buildings, metal mining, or battery manufacturing.
In children, accidental ingestion of lead containing pain causes devastating neurologic consequences.
There are many case reports of inadvertent exposure to lead from pipes, cookware, dishes, cosmetics, retained bullets, moonshine liquor, and herbal supplements.
Most Americans have detectable blood levels.
Lead exposure in the United States persists because of industrial use of, glazed pottery, folk remedies, candy and drinking water.
Industries with the highest numbers of lead exposed workers include battery manufacturing, smelting, refining of non-f2242ous metals, painting and paperhanging.
The most common non-occupational exposures to lead are from shooting firearms, remodeling, renovating, painting, retained bullets and lead casting.
Lead poisoning causes a range of nonspecific symptoms, which depends on the blood level.
Adults with blood lead levels between 30 and 50 µg per deciliter can have mild symptoms including fatigue, irritability, and headache.
More severe symptoms of scene in high lead levels of 70 ng/dL or greater and can include anemia, constipation, colicky abdominal pain, and peripheral neuropathy.
If lead levels are higher than 100 µg per deciliter, cerebral edema, encephalopathy, or death can occur.
Long-term exposure to lead to Burton’s lines on gums, cognitive impairment and motor weakness in arms and legs with common abnormalities of normocytic or microcytic anemia, basophilic stippling, an abnormal kidney or liver function.
Chelation therapy is considered in children with the blood lead level of 45 mcg/dL or greater.
Lead contaminated opium has led to lead poisoning primarily in the Middle East.
Evidence is insufficient to assess the balance of benefits and harms of screening for elevated blood lead levels in asymptomatic children.
Lead poisoning should be considered in any patient presenting with signs and symptoms of porphyria.
Treatment includes removal of the source of lead exposure, oral calcium and iron supplementation for iron deficient patients, and chelation therapy for patients with very high lead blood levels.
While lead collation is effective in reducing the body lead burden, findings regarding the effects on health outcomes remain inconsistent.
Screening high risk children and adults for lead poisoning is recommended and indicated for individuals with suspected exposure and those with unexplained symptoms consistent with lead poisoning.