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Lead Toxicity Clinical Presentation

  • Author: Pranay Kathuria, MD; Chief Editor: Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS  more...
Updated: Feb 08, 2016


The clinical presentation varies widely, depending upon the age at exposure, the amount of exposure, and the duration of exposure. Organic lead, because of its higher lipid solubility, causes greater toxicity and affects the neurological system predominantly. Younger patients tend to be affected more than older children and adults, because lead is absorbed from the gastrointestinal (GI) tract of children more effectively than from that of adults.

Neurological Toxicity

The neurological system is most vulnerable to lead toxicity.  Children are more likely to develop central nervous system toxicity while the peripheral nervous system is more often affected in adults.

The manifestations in children include temperamental lability, irritability, behavioral changes, hyperactivity or decreased activity, loss of developmental milestones and language delay. Lower IQ and ADHD like symptoms may be present. Severe toxicity can cause delirium, convulsions and encephalopathy. Depression and anxiety are more common in patients. Lead causes demyelination of the peripheral nervous system and the abnormalities mostly affect the extensor motor nerves and may result in hand and foot drop.

Hematological Toxicity

Anemia may develop with lead poisoning due to impaired synthesis of heme, hemolysis of red cells and shortened red cell survival. Anemia is usually mild and is more commonly seen in adults.

Gastrointestinal Toxicity

Patients may develop lead colic, nausea, vomiting and anorexia.  Occasionally, some patients with acute poisoning can develop severe diarrhea and dehydration.

Renal Toxicity

Acute nephropathy manifests with tubular defects, which may include phosphaturia, glucosuria and amino aciduria. This combination of tubular defects is referred to a Fanconi’s syndrome. Chronic lead nephropathy is characterized histologically by chronic interstitial nephritis and is frequently associated with hypertension and gout. Furthermore, lead exposure, at much lower levels than those causing lead nephropathy, acts as a cofactor with more established renal risk factors to increase the risk of chronic kidney disease and the rate of progression. Adverse renal effects have been reported at mean blood lead levels of less than 5 mcg/dL. Cumulative lead dose has also been associated with worse renal function.

Cardiovascular Toxicity

Lead exposure has been associated with the development of hypertension. The development of hypertension may be secondary to oxidative stress or an association with chronic nephropathy. Studies have also documented an association between lead toxicity and cardiovascular disease and stroke.

Reproductive Effects

In men, lead causes a reduction in libido, abnormal spermatogenesis, chromosomal damage and infertility. Women experience an increase in the incidence of stillbirth, miscarriage, pregnancy induced hypertension and prematurity.


No pathognomonic symptoms exist. When symptoms do occur, they are typically nonspecific. Consider lead poisoning whenever a small child presents with peculiar symptoms that do not match any particular disease entity. Common nonspecific symptoms include the following:

  • Temperamental lability, irritability, behavioral changes
  • Hyperactivity or decreased activity
  • Loss of developmental milestones, language delay

More significant exposure to lead may cause symptoms in children that are more likely to lead to a medical evaluation. They are as follows:

  • Abdominal pain, loss of appetite, vomiting, constipation
  • Headache, ataxia, somnolence
  • Lethargy, seizures, stupor, coma

The presence of fever does not rule out the diagnosis, which still must be given full consideration.

Inquiries should be made regarding possible sources of lead exposure. For example, query families about the condition of the home, the presence of peeling or cracking paint and plaster, the occupations or hobbies of the family members, and the presence of industry in the immediate vicinity.

Determine the approximate age of the home. Homes built from 1920 to 1950 are more likely to contain lead pigment-based paint than newer homes. Houses built after 1978 are unlikely to contain lead-pigmented paints. Lead contamination still may be present in plumbing fixtures, but the lead dose in plumbing fixtures is an order of magnitude less than that of paint.

Determine whether the home contains any lead-based kitchen utensils, pottery, or imported toys. In addition, inquire about other homes where the child stays, and determine whether a parent is working as a painter or renovator or in a battery factory, shooting range, or other workplace where that lead is used.

Ask about exposure to foods and additives produced outside the United States. Some spices or food coloring may also contain lead pigments, and some candies have been reported to be contaminated with lead. Also ask about the use of herbal folk remedies. Hispanic and Asian families occasionally use herbal folk remedies that may contain lead.

Investigate the patient’s past medical history, including developmental milestones or delays, hygiene, pica, and previous exposure to lead. Evidence suggests that delayed weaning is associated with excessive pica and lead poisoning. It is commonly found that lead-poisoned children are bottle-fed for protracted periods. Inquire about the patient’s siblings (eg, ages, developmental history, school performance, and blood lead levels [BLLLs] if known).


In adults, similar symptoms may develop, although cognitive changes may be discerned more easily, especially since exposures are more typically acute. In addition, adults with chronic exposure may develop other symptoms, such as the following:

  • Weakness of extensor muscles (eg, foot drop, wrist drop)
  • Delirium, hallucinations

Adults with lead poisoning frequently have sleep disorders. They may be hypersomnolent or have difficulty falling asleep at the appropriate time.

A meticulous environmental history is necessary in patients with suspected lead exposure. Depending on whether it is tailored to children or adults, it should include the following information:

Inquire about present and recent residences, including the location, age, and condition of the building; any history of renovations, inspections, or deleading programs; and any analyses of indoor and outdoor surfaces, water, and soil (if available). Ask about practices concerning changing of clothes and the presence of any work areas in the home.

In adults, obtaining a careful occupational and hobby history is important. More than 900 occupations have been associated with cases of lead poisoning. Always ask patients not just the name of their job but also the duties the job entails. This may uncover an obvious cause of exposure.

A history of ingesting illicit liquor may be an important clue to the etiology of lead poisoning. According to a study from a large urban emergency department (ED) involving patients who reported ingesting “moonshine” sometime during the previous 5 years, 51% had elevated BLLs, and 31% had BLLS in the very elevated range (ie, ≥ 50 µg/dL).[19]

Additionally, numerous reports document lead poisoning resulting from retained bullet or shrapnel fragments; thus, a history of military or other penetrating trauma may be important.


Physical Examination

Subtle changes in cognitive performance are not identified easily on physical examination. Careful mental status examination may detect changes in more severe cases, while formal neuropsychological testing may be needed to detect changes in other cases.

A child with lead toxicity is frequently iron deficient and pale because of anemia. The child may be either hyperactive or lethargic.

Impaired fine-motor coordination[20] or subtle visual-spatial impairment may be seen. In adults, chronic distal motor neuropathy (eg, foot drop or wrist drop) may be seen with decreased reflexes and weakness of extensor muscles; sensory function is relatively spared (see the image below). This is a classic, though not very common, presentation of occupational lead toxicity.

Wrist drop in adult with lead poisoning and renal Wrist drop in adult with lead poisoning and renal failure.

It is important to evaluate the patient for papilledema, cranial nerve abnormalities, and signs of increased intracranial pressure (ICP). Cranial nerve involvement, particularly involvement of the optic nerve, is not uncommon. Chronic lead exposure has been shown to cause optic neuritis and blindness.[21]

Lead lines appearing on gingival tissue (see the image below) are very unusual in children. The dentition of children does not promote poor enough hygiene to produce pyorrhea and the subsequent precipitation of lead sulfide. Adults with poor dental hygiene may demonstrate this characteristic finding in any heavy metal poisoning.

Lead line on gingival border of adult with lead po Lead line on gingival border of adult with lead poisoning.

A report indicates that relative hypertension is related to elevated lead levels, but this finding has never been duplicated.

Lead exposure can precipitate a gout attack. The patient should be observed for joint changes suggestive of acute arthritis. In patients with history of penetrating or military trauma, gunshot wounds must be identified.



Lead poisoning, with or without encephalopathy, may result in neurologic, renal, hepatic, or cardiac damage. All organ systems may be potentially damaged by lead. A possibility that symptoms may progress with chelation exists, and the treating physician must be prepared to manage them. Such complications may consist of syndrome of inappropriate excretion of antidiuretic hormone (SIADH), increased ICP, renal impairment from the chelated lead complex, and hypertension.

Nervous system

Neuropsychiatric problems, impaired cognition, learning difficulties, and antisocial behavior are described in both children and adults.

Peripherally, lead selectively affects motor axons, causing segmental demyelination and axonal degeneration. The upper extremities are affected more often than the lower extremities, and extensors are affected more often than flexors. Hand drop and foot drop are common manifestations of axonopathy.


An increased prevalence of renal adenocarcinoma is reported among lead workers. Variability in individual susceptibility may be explained by differences in lead-binding proteins.


Inhibition of enzymes in the heme synthetic pathway, including aminolevulinic acid synthase, delta-aminolevulinic acid dehydratase (ALAD), and ferrochelatase, causes anemia. With kidney disease, erythropoietin production is impaired and thus causes anemia.


Lead can interfere with bone development, leading to the formation of lead lines at bone metaphyses. These lines represent periods of growth arrest, not lead toxicity per se.

Lead interferes with the conversion of 25-hydroxy vitamin D to 1,25-dihydroxy vitamin D and causes rickets or osteomalacia. Patients with Fanconi syndrome may develop vitamin D–resistant rickets.

Reproductive system

Lead is a known reproductive toxin. In males, it causes reductions in sperm count and fertility. In females, it increases the risk of spontaneous abortions, stillbirths, and preterm births. Offspring may experience lead poisoning in utero and may have developmental delay. Research has demonstrated that these reproductive effects occur at relatively low levels of exposure, even those previously considered safe. Skeletal lead may be mobilized during pregnancy and lactation and can be transported to the fetus or the neonate.

Contributor Information and Disclosures

Pranay Kathuria, MD FACP, FASN, FNKF, Professor of Medicine, Director, Division of Nephrology and Hypertension, University of Oklahoma School of Community Medicine

Pranay Kathuria, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Heart Association, American Society of Hypertension, American Society of Nephrology, National Kidney Foundation

Disclosure: Nothing to disclose.


Adam K Rowden, DO Assistant Professor of Emergency Medicine, Jefferson Medical College of Thomas Jefferson University; Director, Division of Toxicology, Department of Emergency Medicine, Albert Einstein Medical Center; Consulting Toxicologist, Children's Hospital of Philadelphia

Adam K Rowden, DO is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, American College of Osteopathic Emergency Physicians, American Osteopathic Association, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Rika Nagakuni O'Malley, MD Instructor, Department of Emergency Medicine, Thomas Jefferson University Hospital

Disclosure: Nothing to disclose.

Chief Editor

Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS Professor Emeritus of Neurology and Psychiatry, Clinical Professor of Medicine, Clinical Professor of Family Medicine, Clinical Professor of Neurosurgery, State University of New York Upstate Medical University; Neuroscience Director, Department of Neurology, Crouse Irving Memorial Hospital

Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS is a member of the following medical societies: American College of International Physicians, American Heart Association, American Stroke Association, American Academy of Neurology, American Academy of Pain Medicine, American College of Forensic Examiners Institute, National Association of Managed Care Physicians, American College of Physicians, Royal College of Physicians, Royal College of Physicians and Surgeons of Canada, Royal College of Surgeons of England, Royal Society of Medicine

Disclosure: Nothing to disclose.


David A Griesemer, MD, Professor, Departments of Neuroscience and Pediatrics, Medical University of South Carolina

David A Griesemer, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine, American Academy of Neurology, American Epilepsy Society, Child Neurology Society, and Society for Neuroscience

Disclosure: Nothing to disclose.

Christopher P Holstege, MD Associate Professor of Emergency Medicine and Pediatrics, University of Virginia School of Medicine; Director, Division of Medical Toxicology, Center of Clinical Toxicology; Medical Director, Blue Ridge Poison Center; Associate Medical Toxicology Fellowship Director, Veterans Affairs Department of Health

Christopher P Holstege, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, European Association of Poisons Centres and Clinical Toxicologists, Medical Society of Virginia, Society for Academic Emergency Medicine, Society of Toxicology, and Wilderness Medical Society

Disclosure: Nothing to disclose.

J Stephen Huff, MD Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine

J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Jonathan S Rutchik, MD, MPH Assistant Professor, Department of Occupational and Environmental Medicine, University of California at San Francisco

Jonathan S Rutchik, MD, MPH is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Occupational and Environmental Medicine, and Society of Toxicology

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

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Peripheral smear taken from 8-year-old Pakistani girl who presented with acute hemolytic anemia and lead level of 125 µg/dL.
Growth arrest lines, also known as lead lines, in bones of child who recovered from lead poisoning.
Lead line on gingival border of adult with lead poisoning.
Wrist drop in adult with lead poisoning and renal failure.
Abdominal flat plate showing multiple radiopaque foreign bodies, including paint chips and earring.
Kidney biopsy results from patient with chronic lead nephropathy show nonspecific tubular atrophy and interstitial fibrosis. Note absence of interstitial infiltrate. Single glomerulus included in section is normal. Image courtesy of Vecihi Batuman, MD, FACP.
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