Approach

The diagnosis of lead poisoning should be considered in any person potentially exposed to lead. Any detectable lead level is consistent with exposure to lead. A blood lead reference value of ≥0.17 micromoles/L (3.5 micrograms/dL) is used to identify children with the highest blood lead levels (within the top 2.5 % of US children aged 1-5 years from 2015-2016 and 2017-2018 National Health and Nutrition Examination Survey [NHANES] cycles).[47] A case definition for an elevated blood lead level in an adult (person ≥16 years of age) is ≥0.24 micromoles/L (5 micrograms/dL).[2][3] In an adult, the US Occupational Safety and Health Administration considers a blood lead level of ≥1.2 micromoles/L (25 micrograms/dL) to be serious, requiring inspection.[2]

A history of exposure is the strongest suggestive feature, as symptoms are non-specific or may be absent. Lead toxicity may be identified during routine screening. Whole-blood lead measurement is the primary method of diagnosis, although interventions should begin at the first sign of increased exposure.

Although spot and 24-hour urine collections (often labelled heavy metal screens) are often requested by clinicians to diagnose lead toxicity, these tests do not add to diagnosis and are not recommended.

History

The main aim of the history is to thoroughly assess the risk of lead exposure. Key features include the following.

  • Age of patient: lead exposure peaks in children at age 18 to 24 months. All children in this age group should be considered for lead testing.[6]

  • Pica: a medical disorder in which children develop an appetite for non-nutritive substances. If the substances consumed contain lead, this may be a significant source of lead exposure.[39][40] Pica is strongly associated with iron deficiency, which is believed to drive the abnormal appetite.

  • Age and condition of housing: lead use in paints has been phased out in many countries, and most lead exposure occurs in housing built before 1950. Paint deterioration increases lead exposure. Screening of children (12 to 24 months of age) for elevated blood lead concentrations is recommended in communities or census block groups with ≥25% of housing built before 1960.[48]

  • Socioeconomic status: patients with a low socioeconomic status are more likely to live in older and poorly maintained buildings, in which the risk of lead exposure is higher.

  • Occupational history: there are multiple lead-hazardous occupations. In larger companies (e.g., battery production or construction), workers should be monitored for lead exposure. Small-business workers, such as painting contractors and plumbers are also at risk, but are not usually tested by their employers.[9][13]​​[49]

  • Hobbies: certain hobbies such as constructing stained glass items that are soldered with lead materials, and making bullets and fishing sinkers in the home, often expose the hobbyist to high levels of airborne lead.[6][13] Self-renovation of an older property may also result in exposure to airborne lead.

  • Dietary history: diets low in minerals, especially calcium and iron, or high in fat, likely increase absorption of lead.[6][23][33] Pre-existing iron deficiency and other mineral deficiencies also increase the absorption of lead from the gastrointestinal tract.[23] The quality of the diet should be determined with particular attention to the mineral and fat content.

  • Use of folk medications: Mexican folk remedies (e.g., azarcon and greta), pay-loo-ah (a Hmong folk remedy), and Ayurvedic medicines have resulted in lead toxicity.[10][11][15][16] Some ethnic groups are reluctant to reveal such use to conventional physicians.[6]

  • Family history of lead poisoning: several children in a family often have common exposures. Housing is the most common source, but lead workers can also bring lead home on clothing.[50]

Physical examination

Most patients are asymptomatic and are identified as part of a screening programme or because a high-risk history of lead exposure is identified. Clinical examination is usually unremarkable.

The key symptoms of lead toxicity are neurological and can affect either the central or peripheral nervous system. Although lead toxicity can cause a microcytic anaemia, this is uncommon in the absence of other risk factors such as iron deficiency anaemia, and its absence does not rule out lead toxicity.

Extremely severe lead poisoning has been associated with renal Fanconi's syndrome, particularly in children. It produces a range of cardiovascular toxicities in adult patients. The key toxicity is hypertension, but coronary artery disease, increased stroke mortality, and peripheral artery disease are also seen. Lead toxicity should be suspected in hypertensive patients with a history of possible lead exposure. Agency for Toxic Substances and Disease Registry: case studies in environmental medicine: lead toxicity Opens in new window

Adults commonly present with colicky abdominal pain, and lead toxicity should be considered in any patient in whom this symptom is persistent and unexplained. Peripheral neuropathies can also occur in adults.

Neurological symptoms

Nervous system examination may reveal peripheral neuropathy or cerebellar signs such as intention tremor, past-pointing, or dysdiadochokinesia.

In children, headaches, loss of appetite, constipation, agitation, somnolence, or clumsiness are signs of central nervous system (CNS) toxicity that require urgent treatment, as they may progress to encephalopathy. Lead encephalopathy is a medical emergency that presents with altered mental state ranging from subtle alterations in level of arousal and behavioural abnormalities to coma. Patients with lead encephalopathy may develop seizures.

Lead-induced CNS damage in children causes cognitive impairment, which can lead to learning difficulties and delay in reaching developmental milestones. Previously achieved milestones may also regress. Hyperactive and inattentive behaviour can also occur, although this is less commonly caused by lead exposure.

Childhood lead exposure has been associated with long-term consequences in adult life, including lower cognitive function, decline in IQ, psychopathology, and low socioeconomic status.[51][52][53] Lifetime lead exposure can be expressed later in life, where it may accelerate the rate of decline in cognition.

Whole-blood lead measurement

The measurement of whole-blood lead is diagnostic. Any detectable lead level is consistent with exposure to lead.

A rise in whole-blood lead from 0.1 micromoles/L (2-3 micrograms/dL) to 0.5 micromoles/L (10 micrograms/dL) results in a significant loss of IQ in children; the loss is more pronounced at these concentrations than at levels above 0.5 micromoles/L (10 micrograms/dL).[27][28][30][54] However, most environmental interventions at these lower levels have not been demonstrated to decrease blood lead, so prevention is key to preventing this IQ loss.

Diagnostic and therapeutic interventions become more intense as the blood level rises above these thresholds. Plasma or serum lead determinations, although useful in determining the available unbound lead, are not used for diagnosis because they are technically difficult and not widely available.[6][13]

The US Occupational Safety and Health Administration publishes blood lead level reference guides and regulatory recommendations related to adult lead exposure in the workplace.[2]

Urinary lead measurement

Urinary lead is measured during chelation therapy to judge the efficiency of chelation by comparing lead-to-chelant ratios. Adequate chelation is defined as a ratio of more than 1 microgram lead to 1 milligram of chelant.[6][13]

Other investigations

A full blood count and ferritin are used to exclude associated iron deficiency anaemia.

Plain radiographs of the abdomen are recommended if lead ingestion is suspected. Radio-opaque material is not usually observed in the abdomen of children on plain films, but when present it indicates the need to evacuate the gut of the material.[6]

Plain radiographs of long bones have previously been recommended in the diagnostic evaluation of paediatric patients, but their value is uncertain. 'Lead lines' in long bones represent growth arrest and are not specific for lead exposure.[55] Furthermore, they are not always present even in heavily exposed children.

Electrophysiology studies are particularly useful in adults with peripheral neuropathies. Nerve conduction studies can document the defects and can be used to follow disease progression.

Emerging investigations

X-ray fluorescence of long bones can estimate long-term exposure to lead using a direct measurement of lead in bone. This has been an exceptionally useful research tool in defining adverse effects of long-term exposure, and this remains its principle use. The high cost and lack of interlaboratory standardisation of methods and results have limited its clinical application.[56][57]

Lead exposure, including during childhood, has been associated with altered brain structure and function.[58][59][60] MRI scanning can be considered; it may show decreased brain volume and alterations in myelination and axonal integrity.[61]

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