Lead and children

Health effects of lead

Lead is a developmental neurotoxin, interfering with neurotransmission, cellular migration, and synaptic plasticity during central nervous system development.1 Children are more vulnerable than adults to the effects of lead for several reasons: they are exposed more often by hand-mouth behaviour and spend time on dusty floors; they absorb lead more efficiently from the gastrointestinal tract (40% vs 5% to 15% for adults),2 a capacity increased by concurrent iron or calcium deficiency1; and their blood-brain barrier and liver detoxification systems are biologically immature.1

Exposure to lead has been associated with many cognitive and motor deficits (eg, deficiencies in reading and math skills, fine and gross motor skills, and memory) and distractibility and other characteristics of attention deficit hyperactivity disorder.3–6 Epidemiologic studies show associations between even low blood lead levels (BLLs) and lowered intelligence quotient (IQ).5

Higher BLLs (and higher lead body burdens measured by levels in bones and teeth) are associated with adolescent delinquent behaviour, poor educational outcomes, reduced adult brain volume, and increased criminal arrests.5,7–11 Clinical symptoms such as anemia, abdominal pain, or neurologic deficits are rare and occur only at very high BLLs. Because lead crosses the placenta and accumulates in fetal tissue, fetuses are especially vulnerable to lead-related neurologic injury.12

Measuring BLLs is the best available way to determine lead exposure. Measuring BLLs accurately reflects recent exposures but poorly captures the cumulative body burden. There is no practical, clinically available measure of lead body burden.13,14

Blood lead levels are measured and reported differently in Canada and the United States (Table 1). The US Centers for Disease Control and Prevention (CDC) action level for blood lead is 10 μg/dL (0.48 μmol/L). This level has been recently questioned, because many recent studies demonstrate neurodevelopmental effects below 10 μg/dL, with no lower threshold for injury identified, suggesting that the decline rate (dose-response curve) in IQ scores might be greater at lower doses.1,5,8,15–18

Sources of information

In preparing this article, we searched MEDLINE using terms relevant to lead exposure and poisoning. We reviewed English-language articles published in 2003 to 2008. Most cited studies provide level 2 or 3 evidence.

Home sources of lead exposure

In the United States, 70% of children’s lead exposure is from lead-based paint in the home.19 In Canada, rental housing and paint surfaces are better maintained than in the United States, resulting in less lead exposure. Lead was eliminated from all paint in Canada in 1991, and Canadian regulations have limited concentrations in interior paint since 1978. Half of Canadian dwellings predate 1970 and would still have lead paint,20 likely covered by lead-free paint. Lead is liberated in dust or chips from paint in poor repair, or during renovation activities including sanding or heat-stripping; children are exposed by ingesting lead-containing paint dust or chips. Children with developmental delays are at higher risk of lead ingestion and are more likely to present with lead poisoning after age 3.1

The remaining 30% of elevated BLLs in US children are from nonpaint sources,19 including soil around homes (from exterior paint, nearby highways, or industries), toys, food, and herbal products. Recently, many children’s toys, including brands such as Thomas and Friends Wooden Railway, Batman, and Dora the Explorer, have been withdrawn from the market because of high lead content, usually in the paint. Any recalled toys should be discarded. Food is a less common source, but lead-soldered pots or lead-containing glazed pottery and crystal glassware occasionally contaminate food.21 Lead sources are listed in Table 2.1,13

Childhood lead exposure from drinking water has been in the news recently.22,23 Drinking water in many older Canadian homes and schools with original plumbing contains lead, which leaches from lead service connection pipes outside the home and lead-soldered plumbing inside the home. Lead pipes were used in “well-built” homes until the 1920s, and 50%-lead solder was used until the late 1980s.24 Although lead in drinking water can occasionally cause serious exposure,23 its levels are generally low.22,24 Tests for lead in water can be done through public health units or private water testing companies.25

Public health interventions, such as removing lead from gasoline, paint, plumbing supplies, and food and drink cans, have successfully reduced children’s BLLs. The percentage of US children with BLLs above 0.48 μmol/L (10 μg/dL) dropped from 77.8% to 1.6% between 1980 and 2002.1 Less than 1% of adult Canadians have BLLs above 0.48 μmol/L (10 μg/dL).26 No population-based data are available for Canadian children younger than age 6; children in only 3 communities having been studied. Children in Vancouver, BC, were found to have a mean BLL of 0.29 μmol/L in 1989; 8% of this sample had levels greater than 0.48 μmol/L.27 Emissions from a large lead-zinc smelter in Trail, BC, contaminated local air and soil, raising childhood BLLs; a childhood lead-exposure prevention program, in which improved technology reduced smelter emissions, reduced children’s mean BLLs to 0.28 μmol/L (5.9 μg/dL) by 1999.28 A small study of 5-year-old Inuit children from Nunavik showed mean BLLs of 0.26 μmol/L (5.3 μg/dL).3

Immigrant or adopted children from countries with higher endemic lead exposures might have elevated BLLs and should be considered to be high risk. Information on high-risk countries can be found in the CDC tool kit, CDC Lead Poisoning Prevention in Newly Arrived Refugee Children.29

Screening

Because post-exposure treatment cannot reverse the cognitive effects of lead exposure, prevention is essential. The Rourke Baby Record recommends screening questions for lead exposure at 12 months and 2 years of age (Box 1).30

The CDC criteria for high-risk groups meriting screening include those identified by the first 3 Rourke Baby Record questions (although the cutoff date for housing is 1978) but add the following:

• children living near lead smelting or processing plants, battery recycling facilities, or other point sources of lead contamination;

• children having parents or other household members with lead-related occupations or lead-related hobbies (eg, pottery and furniture refinishing); and

• all refugee children aged 6 months to 6 years, within 3 months of arrival and again in 3 to 6 months.29

There are no Canadian screening guidelines, although in 1995 the Canadian Task Force on Preventive Health Care found fair evidence supporting targeted screening in high-risk children and infants (B recommendation), but insufficient evidence to recommend for or against universal screening (C recommendation).31

Screening questions have some limitations. All 4 questions in the Rourke version target the 70% of children whose lead exposure comes from household paint. The US version was validated in a suburban population, and the questions might not be generalizable to other groups or regions.32

Office approach to prevention

During preconception counseling, antenatal appointments, or well-baby checkups, family physicians can educate parents about avoiding lead-exposure risks. A patient handout on protecting children from lead is available from CFPlus.*

What should be done?

John’s BLL should be retested immediately to confirm the results, and complete blood count and ferritin levels should be tested to rule out iron deficiency.14

A careful exposure history38 should be taken to rule out nonpaint lead exposures. In this case, the only source of lead exposure was high-lead paint, applied before 1978, liberated by interior renovations and in deteriorating condition on the porch. Hand-mouth activity, with ingestion of lead in dust, was the exposure route for this child.

To prevent continuing exposure, John must immediately be removed from the home until the home has been cleaned up or the situation has abated.1 The Canada Mortgage and Housing Corporation provides careful advice on work-site cleanup and managing deteriorating paint.24 Public health inspectors can perform home inspections and dust-wipe testing to confirm dust as a source of lead exposure.

If the child is iron deficient, iron supplementation (4 to 6 mg/kg daily) can be neuroprotective by reducing gastrointestinal lead absorption. Calcium and zinc supplementation might also be indicated.1

Chelation to decrease BLLs by promoting urinary lead excretion is not indicated for BLLs below 2.16 μmol/L (45 μg/dL)1,39 and should only be done by pediatricians experienced in such treatment. Blood lead levels naturally decline over time, but the half-life is long and variable.14

Neuropsychological evaluation and follow-up is suggested for children with levels exceeding 0.96 μmol/L (20 μg/dL).1

Conclusion

There is a long history of progressive reductions of the BLLs in children requiring action, as research has extended the levels associated with poor developmental outcomes ever lower. New research showing considerable neurodevelopmental effects at BLLs well below 0.48 μmol/L (10 μg/dL), the current “level of concern,”14 and the importance of preventing exposure have led to debate about further reducing the level of concern to 0.24 μmol/L (5 μg/dL) or even 0.10 μmol/L (2 μg/dL).5,40–42 A new action level of 0.24 μmol/L (5 μg/dL) has been proposed in the United States. It was estimated this change would reclassify 7.3% of children aged 1 to 5 and 2.8% aged 6 to 11 with BLLs of 0.24 to 0.48 μmol/L (5.0 to 9.9 μg/dL) to a group requiring evaluation and treatment,42 creating new health care and housing remediation expenses. However, there is a powerful economic argument for lowering lead action levels: lower IQs associated with lead exposure are strong indicators of future lost earning power and antisocial behaviour.11,43

Because the interventions that reduce high BLLs have not been proven effective in preventing neurocognitive deficits, screening is considered too little too late. Preventing exposure through office-based and public education about the hazards of lead exposure is optimal.