^

Health

A
A
A

Lead poisoning (saturnism)

 
, medical expert
Last reviewed: 07.07.2025
 
Fact-checked
х

All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.

We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.

If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.

In lead poisoning, often minimal symptoms at first may progress to acute encephalopathy or irreversible organ dysfunction, and usually result in cognitive deficits in children. Diagnosis is by whole blood lead concentration. Treatment involves discontinuing lead exposure and sometimes chelation therapy with succimer or sodium calcium edetate, with or without unithiol.

Lead paint was widely used until the 1960s, less so in the early 1970s, and was phased out by 1978. Thus, lead paint still poses some risk in older homes. Lead poisoning is usually caused by ingestion of loose, flaking pieces of lead-containing paint. During home renovation, patients may be exposed to significant amounts of airborne lead that accumulated during surface preparation for repainting. Insufficiently coated lead ceramics, commonly outside the United States, may leach lead, especially when the ceramic comes into contact with acidic substances (e.g., fruit, cola, tomatoes, cider). Lead-contaminated homemade whiskey or folk remedies may be a source of poisoning, as may accidental ingestion or tissue contamination of foreign lead objects (e.g., bullets or fishing weights). Bullets in soft tissue can increase blood lead levels, but this process takes years. Occupational exposures include battery making, recycling, bronzing, copper making, glass making, pipe cutting, soldering and welding, smelting, pottery, and dyeing. Some ethnic cosmetics and imported herbal remedies contain lead and can cause outbreaks of lead poisoning in visitors. Fumes from leaded gasoline (not found in the U.S.) inhaled by people who use lead contain lead and can cause poisoning.

trusted-source[ 1 ], [ 2 ], [ 3 ]

Symptoms of Lead Poisoning (Saturnism)

Lead poisoning is most often a chronic condition and may not cause acute symptoms. With or without acute symptoms, poisoning eventually has irreversible effects (e.g., cognitive impairment, peripheral neuropathy, progressive renal failure).

The risk of cognitive impairment increases when whole blood lead concentrations are >10 μg/dL (0.48 μmol/L) over a long period of time, although they can occur at lower concentrations. Other symptoms (eg, abdominal cramps, left flank pain, constipation, tremor, mood changes) are possible at blood lead concentrations >50 μg/dL (>2.4 μmol/L). Encephalopathy occurs at blood lead concentrations >100 μg/dL (>4.8 μmol/L).

In children, acute lead poisoning can cause irritability, decreased attention, and acute encephalopathy. Cerebral edema develops after 1-5 days, causing persistent severe vomiting, ataxic gait, changes in consciousness, severe convulsions, and coma. Encephalopathy may be preceded by several weeks of irritability and decreased play activity. Chronic lead poisoning in children can cause mental retardation, seizures, aggressive behavior, developmental delays, chronic abdominal pain, and anemia.

Adults with occupational poisoning typically develop symptoms (eg, personality changes, headache, abdominal pain, neuropathy) several weeks or later. Encephalopathy is uncommon.

In children and adults, anemia is possible because lead interferes with the normal formation of hemoglobin. In children and adults who inhale tetra-ethyl- or tetra-methyllead (from leaded gasoline), toxic psychosis may occur in addition to the more typical symptoms of lead poisoning.

Symptoms and treatment of typical complications

Poisoning

Symptoms

Treatment

Anticholinesterase inhibitors

Angioedema, arterial hypotension

Activated charcoal; supportive care; for angioedema, epinephrine, antihistamines, or glucocorticoids may be effective

Acephate

See FOS

-

Paracetamol

See paracetamol poisoning in the relevant section

Acetanilide

Aniline dyes and oils

Chloroaniline

Phenacetin (acetophenetidine, phenylacetamide)

Cyanosis due to the formation of met- and sulfhemoglobin, dyspnea, general weakness, dizziness, angina, rash, vomiting, delirium, depression, respiratory and circulatory failure

Ingestion: Activated carbon, then as for inhalation. Skin contact: Undress and wash with soap and water, then as for inhalation.

Inhalation: O2 , respiratory support; blood transfusion; in case of severe cyanosis, methylene blue (methylthioninium chloride) solution at a dose of 1-2 mg/kg intravenously

Acetic acid

Low concentration: moderate irritation of mucous membranes.

High concentration: see caustic poisoning

Maintenance treatment with lavage and dilution

Acetone

Ketones

Glues or cements for toy models

Nail polish solvents

Ingestion: As for inhalation, except for direct action on the lungs. Inhalation: bronchial irritation, pneumonia (pulmonary congestion and edema, weakening of respiration, dyspnea), intoxication, stupor, ketosis, cardiac arrhythmias.

Remove from source, respiratory support 0 and infusion therapy, correction of metabolic acidosis

Acetonitrile

Cosmetic Nail Tips

Converts into cyanide, causing symptoms typical of cyanide poisoning

See cyanides

Acetophenetidine

See acetanilide

-

Acetylene gas

See carbon monoxide

-

Acetylsalicylic acid

See poisoning with acetylsalicylic acid and other salicylates in the relevant section

Acids and alkalis

See individual types of acids and alkalis (e.g. boric acid, fluorides) and poisoning by corrosive substances or by contact with skin and eyes in the relevant section

Glues or cements for toy models

See acetone, benzene (toluene), petroleum distillates

-

Ethyl alcohol (ethanol)

Brandy Whiskey

Other strong alcoholic drinks

Emotional lability, loss of coordination, hot flashes, nausea, vomiting, loss of consciousness from stupor to coma, respiratory depression

Supportive care, intravenous glucose to prevent hypoglycemia

Isopropyl alcohol

Alcohol cleaners

Dizziness, incoordination, disturbances in the level of consciousness from stupor to coma, gastroenteritis, hemorrhagic gastritis, arterial hypotension, without retinal damage or acidosis

Supportive care, intravenous glucose, correction of dehydration and electrolyte disturbances; in gastritis - intravenous H1-receptor blockers or H,K-ATPase inhibitors

Methyl alcohol (methanol, wood alcohol)

Antifreeze

Paint thinners

Lucky

High toxicity when taken 60-250 ml in adults or 8-10 ml (2 teaspoons) in children; latent period 12-18 hours; headache, weakness, cramps in the calf muscles, dizziness, convulsions, retinal damage, twilight vision, acidosis, weakening of breathing

Fomepizole (15 mg/kg, then 10 mg/kg every 12 hours); alternative treatment: 10% ethanol with 5% glucose or 0.9% sodium chloride intravenously; loading dose of ethanol 10 ml/kg over an hour, then 1-2 ml/kg per hour to maintain blood ethanol concentration of 100 mg/dL (22 mmol/L); hemodialysis (definitive treatment)

Diagnosis of lead poisoning (saturnism)

Lead poisoning should be suspected in a patient with characteristic symptoms, but such symptoms are often vague and the diagnosis is often delayed. Investigations include a complete blood count and determination of plasma electrolytes, blood urea nitrogen, creatinine, and plasma glucose, as well as blood lead concentration. Abdominal radiography is performed to detect radiopaque lead particles. In children, radiographs of the long tubular bones are taken. Horizontal lead bands on the metaphysis, indicating inadequate red blood cell production and increased calcium deposition in the ossification zones of children's bones, are signs of lead or other heavy metal poisoning, although these signs are not absolute. Normocytic or microcytic anemia suggests lead poisoning, especially when the reticulocyte count is elevated or when the basophil granularity in the blood is increased. However, the specificity of these tests is also limited. The diagnosis is reliable if blood lead concentrations are >10 μg/dL.

Because measuring blood lead levels is not always possible and is expensive, other preliminary or screening tests can be used to detect lead poisoning. The capillary blood lead test is accurate, inexpensive, and quick. However, any positive test result should still be confirmed by measuring blood lead levels. Measurement of red blood cell protoporphyrin (also called zinc protoporphyrin or free red blood cell protoporphyrin) is often inaccurate and is rarely used.

The CaNa-EDTA lead mobilization test, previously used for diagnosis and treatment, is considered obsolete by most toxicologists and is not routinely used.

trusted-source[ 4 ], [ 5 ], [ 6 ], [ 7 ], [ 8 ]

Who to contact?

Treatment of lead poisoning (saturnism)

All patients should be isolated from the source of lead. If lead particles are visible on abdominal radiograph, whole-bowel irrigation with an electrolyte solution containing polyethylene glycol is performed at a rate of 1000–2000 mL/h for adults or 25–40 mL/kg/h for children until repeat radiographs show no residual lead. If a bullet is the cause of poisoning, it is removed surgically. Children with blood lead concentrations >70 μg/dL (>3.40 μmol/L) and all patients with neurologic symptoms should be hospitalized. Patients with acute encephalopathy should be admitted to an intensive care unit.

Chelating agents [eg, succimer (meso-2,3-dimercaptosuccinic acid), sodium calcium edetate, unithiol] are used to bind lead into forms that can be excreted from the body. Chelation should be supervised by an experienced toxicologist. Chelation is indicated for adults with symptoms of poisoning and blood lead levels >70 μg/dL and for children with encephalopathy or blood lead levels >45 μg/dL (>2.15 μmol/L). Hepatic and renal impairment are relative contraindications to chelating agents. Chelating agents should not be given to patients who are still exposed to lead because chelation may increase gastrointestinal absorption of lead. Chelation removes only relatively small amounts of metal. If body lead levels are high, the procedure may need to be repeated many times over many years.

Patients with encephalopathy are treated with unithiol at a dose of 75 mg/m (or 4 mg/kg) intramuscularly every 4 hours and 1000-1500 mg/m sodium calcium edetate intravenously once a day. The first dose of sodium calcium edetate should be administered no earlier than 4 hours after the first administration of unithiol to prevent lead from entering the brain. Unithiol administration can be suspended after several doses depending on the lead concentration and the severity of symptoms. Combined treatment with unithiol-sodium calcium edetate is carried out for 5 days, followed by a 3-day washout. The indications for long-term chelation are then reviewed.

Patients without encephalopathy are usually given succimer 10 mg/kg orally every 8 hours for 5 days, then 10 mg/kg orally every 12 hours for 14 days. If symptoms persist, such patients may alternatively be treated for 5 days with unithiol 50 mg/m2 deep intramuscularly every 4 hours plus sodium calcium edetate 1000 mg/m2 intravenously once daily.

Unithiol is given with parenteral or oral fluids because of the risk of vomiting. Unithiol may also cause severe pain at the injection site, numerous systemic symptoms, and, in patients with glucose-6-phosphate dehydrogenase deficiency, moderate to severe acute intravascular hemolysis. This drug should not be given with iron supplements. Unithiol is made from peanut derivatives and is therefore not used in patients with or suspected of having a peanut allergy.

Sodium calcium edetate may cause thrombophlebitis, which can be prevented by administering the drug intravenously rather than intramuscularly at a concentration of less than 0.5%. The urinary tract should be checked for normal function before initiating treatment with sodium calcium edetate. Severe reactions to sodium calcium edetate include renal failure, proteinuria, microscopic hematuria, fever, and diarrhea. Renal toxicity is dose-related and is reversible in most cases. Adverse effects of sodium calcium edetate are most likely due to zinc depletion.

Common adverse effects of succimer include skin rashes, gastrointestinal symptoms (eg, anorexia, nausea, vomiting, diarrhea, metallic taste), and transient increases in liver enzymes.

Patients with blood lead concentrations >10 μg/dL should be carefully evaluated and they or their parents should be advised about lead protection.

Prevention of lead poisoning (saturnism)

Patients at risk should have their blood lead levels measured regularly. Measures that reduce the risk of home poisoning include regularly washing hands, children's toys, pacifiers, and surfaces in the home. Drinking water, indoor paint (except in buildings built after 1978), and ceramics made outside the United States should be tested for lead. People who work with lead should use appropriate personal protective equipment, change boots and clothing before returning home, and shower before bed.

You are reporting a typo in the following text:
Simply click the "Send typo report" button to complete the report. You can also include a comment.