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Lead toxicity with a new focus: Addressing low-level lead exposure in Canadian children

Posted: Jun 21, 2019

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Principal author(s)

Irena Buka, Catherine Hervouet-Zeiber; Canadian Paediatric Society, Paediatric Environmental Health Section

Paediatr Child Health 2019 24(4):293 (Abstract)


Although acute and subacute lead toxicity requiring active treatment is rare in Canada, paediatricians need to be aware of new evidence linking lower lead levels to neurodevelopmental deficits. Health Canada has identified potential exposures occurring prenatally, in infancy and during early childhood from food and water, household dust, soil and mouthing products that contain lead. Children with neurodevelopmental problems who live in older housing and newcomers to Canada may be at greater risk. Symptoms may be latent, subtle and chronic. Blood assay, widely available clinically, does not confirm diagnosis unless lead exposure has been recent. Human biomonitoring data is available in the Canadian Health Measures Survey, and Health Canada has suggested that clinicians use these new reference ranges. Early detection and prevention of lead exposure are key public health objectives because effects of lead toxicity are chronic and treatment is complex.

Keywords: Blood lead levels; Cognitive deficit; Lead exposures; Lead toxicity; Paediatrics

Paediatricians in Canada will rarely encounter acute or subacute lead toxicity marked by headache, abdominal pain, anemia, constipation, vomiting, clumsiness, somnolence, stupor, renal failure, seizures or possible death. That is because important public health interventions have progressively lowered blood lead levels (BLLs) in Canadian children over recent decades. Lead was removed from gasoline in the 1990s, which significantly reduced exposures through inhalation. Lead concentrations from indoor paints used in Canadian homes have also decreased since the late 1950s, both through voluntary industry initiatives and tighter restrictions under the Health Protection Act of 1976 [1]. However, the effects of elevated water lead levels in Flint, Michigan, USA, identified in 2015, were caused by a change in the city’s water source. The resultant ongoing public health crisis is an urgent reminder that aging lead water pipes present in Canada need to be monitored closely [2]. This practice point helps clinicians to identify, assess and manage children at risk for lead exposure as well as to prevent further exposures. It was developed by consensus, based on a review of Canadian studies, Health Canada documents, and publications from the World Health Organization (WHO), United States government resources and other specialist organizations.

While vigilance remains necessary for more severe symptoms of lead toxicity, the focus of care has generally shifted to neurological manifestations at lower doses [3]. Many determinants of health influence neurodevelopmental symptomatology, but lead exposure occurring prenatally and during the first 2 to 3 years of life can have life-long effects. In 2003, the WHO estimated that 3.5% of mild intellectual disability worldwide is caused by lead exposure [4], and a subsequent pooled analysis demonstrated cognitive deficits at BLLs much lower than previously thought to be harmful [3].

Historically, Canada has mirrored progressive lowering of the paediatric “level of concern” for BLLs in the United States, from an initial 40 mcg/dL in 1970, to 30 mcg/dL in 1975, 25 mcg/dL in 1985 and 10 mcg/dL in 1990 [5]. In 2012, the United States Centers for Disease Control and Prevention (CDC) announced a new reference level of 5 mcg/dL, based on the 97.5 percentile of BLLs in children in the United States aged 1 to 5 years [6]. This reference level was adopted by the American Academy of Pediatrics (AAP) in 2016 [7]. One recent study has reported that approximately 3% children in the United States have BLLs ≥5.0 mcg/dL [8].

In 2017, Health Canada released their Fourth Report on Human Biomonitoring of Environmental Chemicals in Canada [9], which evaluated means at selected percentiles of blood and urine lead by age group and gender. One significant limitation of this report, however, is the lack of measurements in children younger than 3 years of age, the most vulnerable population, and the group in whom lead levels are most likely to be elevated.

Potential environmental sources of lead exposure in Canadian children

Children can be exposed to many environmental contaminants simultaneously and on a daily basis, at home, in child care or at school, and elsewhere. There may be a latency period before the effects of exposure are diagnosed. Children are especially vulnerable to environmental exposures because of their rapid growth and development, dynamic physiology and unique behaviours, and the potential for life-long effects.

Lead exposure can start prenatally, from exogenous lead exposures during pregnancy as well as from a mother’s endogenous stores [10]. Following birth, exposure can occur via ingestion, inhalation and/or dermal absorption. Preschool children can absorb approximately 40% of the lead they happen to ingest, while adults absorb only about 10%. Approximately 70% of the body’s stored lead is in bones and can be re-released into the bloodstream during remodelling of bones during childhood, adolescence or old age, or in response to stress, pregnancy or malnutrition [11].

Health Canada has identified the most common potential sources of lead exposure in young children as food and water, household dust and soil, and from mouthing products that contain lead [1][11]. Common foods and beverages contribute approximately 0.1 mcg lead per kg of body weight per day, with higher overall exposures in children. Lead may accumulate in food grown in soil on previous industrial sites or next to old buildings or busy roads, but can also be present in water or air, or introduced in other ways during growth, transportation, preparation and storage. Banning the use of lead solder in food cans in most countries, including Canada, has greatly reduced lead exposure through food. Indigenous peoples who hunt and eat a traditional diet, including meat from animals shot with lead bullets, may be at risk. In older homes and neighbourhoods, tap water may be contaminated by lead pipes installed before 1960 or repaired with lead solder used until the 1980s [11]. See Table 1 for other common sources of lead exposure.

Who is more vulnerable to lead exposure?

Identifying the children most at risk for lead exposure is the first step toward prevention. Consider blood lead testing for children who have [6][12]:

  • Lived in a house or apartment built before 1960 within the past 6 months, especially when water is supplied by lead piping or original paint is present, peeling or chipped, or the dwelling is under renovation.
  • A sibling, housemate or playmate with a history of lead poisoning.
  • Pica or have eaten paint chips, or tend to mouth painted surfaces.
  • Emigrated or been internationally adopted from a country where population lead levels are higher than in Canada.
  • Any of one of the above risk factors, combined with a known or suspected neurodevelopmental disorder.

The most vulnerable subpopulations include children who already a carry higher burden of lead in their bodies (e.g., infants born to mothers who have experienced exposures themselves or lacked divalent minerals (e.g., calcium, magnesium, iron, zinc) during pregnancy)[6][12]. Children exhibiting pica or with a neurodevelopmental deficit such as autism spectrum disorder, and especially if they tend to mouth objects, tend to have higher BLLs [13]. In the United States, African-American or other children living in poverty are particularly vulnerable, because lead exposures from older or deteriorated housing [13] may be combined with having poor nutrition. Shared absorptive pathways cause children with a mineral deficiency (e.g., of calcium, iron and zinc) to absorb more lead [11].

When low-level lead exposure is suspected

Children with low-level lead exposure are often asymptomatic and when symptoms are present, they are usually subtle. Symptoms may include cognitive delay or other neurodevelopmental signs, such as inattention, hyperactivity, hearing impairment, poor balance or speech delay. Consider requesting these laboratory investigations in cases of suspected lead exposure:

  • Blood lead (venous sample)
  • CBC
  • Ferritin
  • Calcium, protein, albumin

Conducting a focused nutritional history and neurodevelopmental assessment with ongoing follow-up are also recommended. When an index case of lead exposure has been identified, consider activating a Paediatric Environmental Health History (PEHH) for other household members or close contacts.

How to confirm lead exposure

Health professionals may order a simple, standardized and inexpensive BLL test for children they suspect are at risk for lead exposure. An elevated venous BLL is the ‘gold standard’ to confirm recent lead exposure, always remembering that the half-life of lead in red blood cells is approximately 45 days. BLLs can decline when exposure ceases, but rather than being excreted, lead moves into other body parts, especially bone. Children’s BLLs typically peak at age 2 to 3 years of age [11]. A current low BLL may not satisfactorily rule out lead as a contributing factor to symptoms, particularly if previously higher levels have not been documented [14]. Testing is still useful for determining recent or ongoing exposures.

Interpreting children’s BLLs

Children found to have a BLL higher than 5 mcg/dL (0.24 mcmol/L) should be investigated thoroughly, and any identified exposure sources should be mitigated as soon as possible. Lead has been recognized as a chemical having no-safe threshold [6] though as noted, the CDC’s reference level of 5 mcg/dL (0.24 μmol/L) was accepted by the AAP in 2016 [6][7]. Canadian clinical laboratories may report BLLs in micromoles per litre. To convert mcmol/L to mcg/dL, multiply by 20.72 (e.g., 0. 483 mcmol/L= 10 mcg/dL).

Investigating children who have been exposed

Once an elevated BLL has been identified, a detailed assessment of the child’s environment must be performed. The lead source may not be obvious or there may be multiple sources of lead. A Paediatric Environmental Health History (PEHH) (Table 1) can help health care providers to identify possible sources of lead exposure.

Table 1. Paediatric environmental health history (PEHH) criteria

Home/Child care/School

  • Neighbourhood established in the 1960s or before, especially if supplied by lead water pipes or if lead solder was used for piping or plumbing fixtures
  • Buildings constructed in the 1980s or earlier, if lead paints are present and especially if exposed areas were painted before 1960
  • Building where child spends time is in a poor state of repair
  • Proximity to a current or past industrial or waste site
  • Proximity to a busy roadway for (<30 yards distant) or an airfield, where small-engine planes approach or take off

Consumer products

  • Costume jewelry
  • Candles (e.g., lead in wicks)
  • Imported painted toys, wax crayons, mini-blinds, vinyl items (e.g., toys, containers, lunch boxes), painted reusable bags
  • Cosmetics (e.g., kohl)


  • Imported sugar, candy and baking supplies
  • Food prepared with, served or stored in containers made of pewter or ceramic (especially with a leaded glaze), or leaded crystal
  • Foods, particularly vegetables in the Brassica family, grains and other foods that may accumulate lead (e.g., dandelion greens growing along busy roadways, or  cabbages or kale grown by the foundation of an old home or in untested inner-city soil)
  • Wild game shot with lead bullets

Occupation and hobby-related

  • Battery manufacturing and recycling
  • Radiator repair, welding
  • Lead mining and smelting
  • Brass and bronze foundry work
  • Demolition and renovations
  • Hunting, marksmanship, military (e.g., a firing range)
  • Pottery glazing
  • Leaded glass

Family factors

  • Mother may have been exposed to lead before or during pregnancy
  • Previously lived in a country or region with higher population lead levels
  • Sibling or other close contact with lead exposure

Adapted from reference [11]

Managing children with lead toxicity

Steps for managing lead toxicity according to BLL are detailed in Table 2. Chelation therapy is only indicated at high BLLs and must be conducted by a physician expert in this area. Treating the effects of low-level lead exposure can be a challenging, costly, lifelong process, with outcomes depending on behaviour-based interventions and care. Potential long-term consequences of both acute and low-dose chronic exposures, including hypertension, vascular disease, renal impairment, and aberrant behaviour [11][15] require close monitoring and follow-up.

The early identification of children at risk allows for more effective responses. Local public health authorities may be helpful for identifying and mitigating exposures.

Table 2. Managing lead toxicity based on blood lead level (BLL) *

5 to 14 mcg/dL

  1. Review lab results with the child’s family.
  2. Perform routine health maintenance, including neurodevelopmental screening, and assess nutrition.
  3. Take a careful PEHH to identify potential sources of exposure (Table 1). Provide preliminary advice about reducing or eliminating exposure source(s).
  4. Contact local public health authority for guidance.
  5. Re-test venous BLL at 1 to 3 months to ensure the child’s lead level is not rising. If it is stable or decreasing, retest in 3 months.
  6. Provide nutritional counselling related to calcium and iron. Recommend having a fresh fruit with every meal because iron absorption quadruples when taken with vitamin C-containing foods. Encourage the consumption of iron-enriched foods (e.g., cereals, meats). Ensure iron sufficiency with adequate laboratory testing (CBC, ferritin, CRP) and treatment. Consider starting a multivitamin with iron.
  7. Complete a full neurodevelopmental assessment and follow-up. Lead’s effects on development may manifest over years.

15 to 44 mcg/dL

  1. Perform steps as described above for BLLs 5 to 14 mcg/dL.
  2. Confirm the BLL with repeat venous sample at 1 to 4 weeks.
  3. Additional, specific evaluation of the child, such as abdominal x-ray should be considered based on the PEHH. Gut decontamination may be considered if ingested foreign objects are visualized on x-ray. Contact your local Poison Centre for assistance. Chelation is not typically recommended for asymptomatic patients.

>44 mcg/dL

  1. Follow guidance for BLLs 15 to 44 mcg/dL.
  2. Confirm the BLL with repeat venous testing at 48 hours.
  3. Consider hospitalization and/or chelation therapy in consultation with your local Poison Control Centre. Mitigating lead exposures at home, identifying other possible sources, assessing the family’s social situation, and chronicity of the exposure will influence management.

* To convert mcmoL/L to mcg/dL, multiply by 20.72. For example: 0.483 mcmoL/L= 10 mcg/dL

CBC Complete blood count; CRP C-reactive protein; PEHH Paediatric environmental health history

Adapted for Canadian use from reference [16]


Low levels of lead exposure can manifest with subtle or severe neurodevelopmental, behavioural and cognitive symptoms. Prevention, early identification, source removal and nutritional measures are key to avoiding chronic and damaging symptomatology. Paediatricians need to be alert to the hazards of low-dose lead toxicity to recognize, assess and manage potential exposures. While chelation is recommended only for high level exposures, identifying and mitigating sources of lower level exposures are important treatment modalities.

Recommended resources


This practice point has been reviewed by the Community Paediatrics and Drug Therapy and Hazardous Substances Committees of the Canadian Paediatric Society. The authors wish to thank previous CPS Paediatric Environment Health Section members and other expert reviews for their input, including Drs. Robin Walker, Alvaro Osornio-Vargas, Hilary Weber, Marie Hay, and Meg Sears, and former CAPHC President, Elaine Orrbine.


Executive members: Faruqa Ladha MD (President), Alvaro Osornio Vargas MD (President-Elect), Catherine Hervouet-Zeiber MD (Past President), Robert Issenman MD (Secretary-Treasurer), Irena Buka MD (Member at large), Arend Strikwerda MD (Member at large), Shazeen Suleman MD (Member at large), Robin Walker MD (Member at large)
Principal authors: Irena Buka MD, Catherine Hervouet-Zeiber MD


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Disclaimer: The recommendations in this position statement do not indicate an exclusive course of treatment or procedure to be followed. Variations, taking into account individual circumstances, may be appropriate. Internet addresses are current at time of publication.

Last updated: Feb 7, 2024