Please note: In 2003, the CTF updated its Grades of Recommendations to include an "I Recommendation" for situations where insufficient evidence exists to allow a recommendation to be made.  (Formerly, these situations were captured under a "C Recommendation".)  This change is not retroactive, and all "C Recommendations" made prior to 2003 have not been reevaluated in light of the new "I" recommendation grade.  For a discussion of these recommendation grades, please link to the 2003 article in the Canadian Medical Association Journal here.

Overview
Lead is a heavy metal that can affect virtually every organ system in the body, particularly the nervous, hematologic and gastrointestinal systems. It is widely distributed throughout the environment because of contamination from energy production, metallurgy and associated processes.

In 199 1, the U.S. Centers for Disease Control and Prevention (CDC) revised their intervention level for lead toxicity from blood lead (BPb) levels of 25 mg/dL to 15 mg/dL.< 1> The CDC now recommends l) screening virtually all children for lead exposure at 12 and 24 months; 2) screening children at high risk every 6 months beginning at 6 months of age; and 3) using direct measurement of BPb rather than erythrocyte protoporphyrin (EP) to screen.

A recommendation for universal screening with BPb assumes that many children have mild ( 10-24 mg/dL) or moderate (25-44 mg/dL) lead exposure, that this condition can be accurately and reliably detected by available screening tests, that the condition is harmful to children, that detection results in meaningful health benefits, and that such benefits outweigh the risks associated with intervention. (Note: The units mg/dL will be used throughout this chapter. To convert to umol/L, divide by 20.72.)

In adapting these criteria to the Canadian context the Canadian Task Force finds fair evidence to support targeted screening by blood lead (BPb) determination in high-risk infants and children (B Recommendation) but insufficient evidence to recommend for or against universal screening in Canada. (C Recommendation).

This review examines published evidence regarding mild and moderate lead exposure in order to determine whether a recommendation for universal screening to detect these levels is supportable in Canada. Studies of adults occupationally exposed to lead were excluded from consideration.

Burden of Suffering
Short-term acute exposure to high levels of lead can cause a metallic taste, abdominal pain, vomiting, diarrhea, convulsions, coma or even death. Long-term exposure may lead to anemia, learning disabilities and hyperactivity, problems with memory and attention span, as well as lack of appetite, abdominal pain, irritability and impaired kidney function.

Prevalence
The prevalence of neurotoxic lead levels in asymptomatic children in Canada is unknown. Surveys which have been conducted in Canada in the last fifteen years revealed that most Canadian children have blood lead levels below 10mg/dL and that the levels of lead exposure have declined. However variations in the reported prevalence of lead exposure in different communities and populations suggest that important local differences may exist. Clinically recognized lead poisoning is a rare event among Canadian children, and chelation therapy is rarely used. Lead poisoning is insignificant when compared to poisoning by other drugs.

In 1978, The Canada Health Survey, the only national survey of blood lead levels in children, reported that 90.3% of boys and 100% of girls aged 3 to 4 years had blood lead levels below 10 mg/dL. In 1986, the Royal Commission on Lead in the Canadian Environment concluded that the blood lead levels for children and adults above the action level of 25 mg/dL were substantially less prevalent in Canada than in the large urban areas of other countries and were the lowest reported for all countries from which comparable data were available. These findings also applied to "hot spots", such as downtown areas, near lead smelters, lead-using industries, mines, concentrators, or other metallurgical industries.

A recent summary of blood lead surveys in Canada from 1979 to 1989 also found that the mean blood lead level in preschool children was less than 10 mg/dL, except in areas where the soil was contaminated.

The Ontario Ministry of Public Health, Public Health Branch have conducted surveys of blood lead levels from 1984 to 1992 in 4-6 year olds in downtown Toronto and estimated that under 4% of Ontario 4-6 year olds were in the 11-14 mg/dL range. They also reported that the mean blood lead levels in this age group had fallen from 12 mg/dL in 1984 to 3.5 mg/dL in 1992. Two recent Canadian studies comparing blood lead levels of pre-school children in smelting towns (Trail B.C., and Rouyn-Noranda, P.Q.) from the mid-1970s to the late 1980s have also reported similar findings, reporting declines of about 45%.

Cross-sectional studies of blood lead levels in urban, suburban and rural Quebec and Ontario children found geometric means of £10 mg/dL.<2,3> In a 1989 study in Vancouver about 7% of preschool children had a blood lead level of 9.94 mg/dL and mean blood lead level was 5.39 mg/dL.

A 1991 cross-sectional study in Saint John, New Brunswick revealed that among 23 children and 68 adults tested, 53% had blood lead levels above 25 mg/dL. A second survey of 205 individuals found that 50 were above 25 mg/dL. In a third study of 97 city children aged 1-3 years, 11.3% of participants had levels above 25 mg/dL. Mean blood lead levels were 4.77 mg/dL (range 1.2 mg/dL-18 mg/dL) in males and 5.6 mg/dL (range 1.4- 17.6 mg/dL) in females.<4>

Studies conducted on neonates in urban Toronto and urban, suburban and rural Quebec reported a geometric mean of <2 mg/dL.<5> Ninety-nine percent of the Toronto infants studied had cord blood lead levels below 7.04 mg/dL as compared to 34% in a similar study conducted in Boston and in Port Pirie, Australia, a high-risk area.

In the U.S., a national survey of BPb levels conducted as part of the National Health and Nutrition Examination Survey II (NHANES II) in 1976-1980 found that average blood lead levels, adjusted for race, sex, age, urbanization, etc., had decreased approximately 37% between 1976 and 1980. This decline correlated significantly with the concurrent decline in the use of leaded gasoline. Wide variations between communities suggested that community rather than national prevalence surveys were required to determine the need for screening and intervention.

Periodic population-based samples of BPb levels from Europe also have shown continuing declines in blood lead levels associated with reductions in the use of leaded gasoline over the past decade.<6,7>

Sources of Lead in the Environment
Sources of environmental lead exposure include: lead-based paint; soil and dust from paint, gasoline, and industrial sources; drinking water; certain occupations and hobbies; airborne lead from point sources such as lead smelters; and lead-contaminated food (from sources such as lead-soldered cans, the rain and soil in which food plants were grown, storage and serving vessels, and dust in the home).<1> Certain traditional ethnic remedies have also been associated with lead exposure.<8>

The individual contributions of each of these lead sources to the overall body burden of lead is not well-defined, primarily because of the lack of large population-based representative samples of concurrent measures of BPb levels and environmental lead exposures. In Canada, the Hazardous Product Act has imposed strict federal legislation which has reduced lead levels in food, interior paint, furniture, and coatings of children’s toys. Lead pipes and solder are prohibited but may still contribute to increased levels of lead in drinking water in areas with highly acidic water.

Paint
In the United States, lead-based paint is thought to be the most common high-dose source of lead exposure for children, and is an important source of household dust lead.<1> By contrast, in Canada, elevated blood lead levels due to lead dust from paint and pica are less commonly reported at levels higher than 10mg/dL, although cases may go undetected and/or unreported. Lead-based paint was in widespread use until the 1950s when the use of lead-based paint and its lead concentration began to decline. The manufacture of leaded paint was banned in Canada in 1972 and in the United States in 1978 although it is still available for industrial, military and marine use.

Although most Canadian experts feel that paint as a source of lead exposure is dramatically less significant in Canada than in the United States, a recent article cautions that "sound scientific data supporting this position are lacking".<2>

Lead paint exposure from housing has been associated with lead toxicity as measured by BPb levels.<4,9,10> Houses built prior to 1950 are the most likely to contain paint with high concentrations of lead. The risks of exposure from leaded paint and household dust are greatest when the paint is in deteriorated condition, as when chipped or peeling. In a recent cross-sectional study, peeling paint was found to be a significant factor associated with elevated blood lead levels in children living in the city of Saint John, New Brunswick.<4>

Remodelling and renovations of older houses can also produce increased levels of lead in the environment, increasing children’s risk of toxicity.

In its 1986 report, the Royal Commission on Lead in the Canadian Environment was unable to identify any case where lead paint was definitely implicated in raised blood lead levels among groups of children. Since then isolated cases of acute lead poisoning with profound sequelae from chronic ingestion of lead-based paint have been reported in London, Ontario, Winnipeg, Manitoba and Halifax, Nova Scotia. Other cases may have occurred but are not easily identified or are asymptomatic.

Air
Blood lead levels of Canadians have shown a consistent decline over the past fifteen years, attributed largely to the removal of lead from gasoline.

Soil
Lead in soil and dust are also important sources of exposure, despite recent declines in its use in paint, gasoline, and industry. Soil lead levels near roadways and adjacent to lead smelters are typically thousands of times higher than natural levels.

Water
Water lead concentration has also been found to correlate with BPb concentrations.<2,11> In the city of Saint John, New Brunswick, it was reported in 1990 that 13% of homes surveyed had lead levels of 50 parts per million (ppm). The acceptable level according to the Canadian Guideline is 0.01 ppm. Blood lead levels have been found to be significantly associated (p<0.05) with living in certain areas of the city, lead pipes from the main water line leading into the home or lead pipes in the home and using hot water directly from the tap in preparing food.<4>

Risk Factors for Increased BPb Levels
Risk factors for elevated BPb levels relate either directly or indirectly to the sources of lead exposure described above. The most important demographic risk factor is probably age. Blood levels tend to rise after birth, peak between 18 months and 2 years of age, and decline gradually through adolescence.<12,13> Possible contributors to this age effect include ingestion of lead in food at a greater quantity relative to body weight compared to adults, increased efficiency of gastrointestinal lead absorption, and normal hand-to-mouth activity in young children that results in their frequently placing their dirty hands and other objects into their mouths.

Several recent cohort studies have attempted to clarify the contributions of various sociodemographic risk factors to BPb levels with conflicting results.<4,14> Given the correlational nature of sociodemographic risk factors, however, it is possible that both lead indices and social factors may be associated with other unmeasured factors related to environment lead exposure. This is particularly important because of their potential role as confounders in evaluating the effects of lead on childhood growth and development, since sociodemographic factors have important independent effects on these outcomes.

Household members may also be exposed to high lead levels from clothing or waste material brought home by workers in lead-based industries or hobbies.<1>

Neurobehavioural Effects of Lead
Exposure to very high levels of inorganic lead associated with blood lead levels >70 mg/dL can cause convulsions and coma, sometimes resulting in death or long-term sequelae.<1> Neurotoxic effects may occur at BPb levels much lower than 80 mg/dL; the threshold (if any) for such effects in humans, particularly children, is unknown. The principal concern of recent research has been the risk of neurodevelopmental dysfunction in children, related to the effects of lead on the immature, rapidly developing nervous system.

Evidence that reductions of moderate BPb levels (25-55 mg/dL) may benefit children’s cognitive function comes from a recent prospective cohort study evaluating chelation therapy and iron supplementation (for iron deficient or depleted children) in 154 children aged 13-87 months, all of whom received "largely successful" household lead abatement.<15> At 6-months follow-up, changes in cognitive function were significantly associated with reductions in BPb level after controlling for confounding variables. The cognitive index increased 1 point for every 3 mg/dL decrease in BPb level over the 6 month period.

No prospective studies evaluating associations between reductions in mildly elevated BPb and improvements in cognition have been identified. There is currently fair evidence that low level lead exposure as measured by BPb has a statistically significant effect on IQ or related measures of cognitive function but the clinical significance is unknown. In the past two decades, many studies<12-39> have evaluated lead exposure (as measured by BPb) and cognitive function in children, but few have found a significant effect of mild to moderate exposure on neurobehavioural function in children. Results from different studies have been inconsistent, effect sizes have been small, and few associations have been statistically significant. Many studies included children with moderate rather than low (10-24 mg/dL) BPb levels. The effects, if any, of low BPb levels on cognition are likely to be even smaller.

It is possible, however that these studies were unable to demonstrate a major effect because 1) intelligence may not be the best measure of neurologic damage due to lead; 2) sample sizes were too small to detect an effect; or 3) BPb may be an inadequate measure of exposure.

BPb levels primarily reflect recent exposure (i.e. over the last 3-5 weeks) and correlate poorly with lead levels in shed deciduous teeth,<17> which may better represent chronic or cumulative exposure. Mean dentine lead levels increase with duration of exposure to high levels of domestic water lead, and with age. Tooth (or dentine) lead may therefore represent cumulative lead exposure, in which case the causal linkage between cognitive function and high tooth lead levels would be clearer than between cognitive function and high BPb levels. Studies of tooth lead therefore may raise fewer methodologic questions than those of BPb, and a number of such studies have recently been conducted. Studies using dentine lead concentrations have shown consistent associations between increased lead and decreased IQ, although effect sizes have been quite small and not always statistically significant,<16,17,40-46> and some of these studies have suffered from methodologic errors.

There is fair evidence that lead exposure as measured by tooth lead is associated with (perhaps not causally) a small reduction in IQ test scores. There is limited evidence that tooth lead is associated with inferior long-term scholastic achievement.<40,41> Studies of the effects of mild lead exposure, as reflected by tooth lead levels, on long-term scholastic achievement need to be replicated. Continued research on the effect of lead on neurobehavioural function, with attention to improved measurement of lead burden and to adequate control of potential confounding, is essential.

One problem with evaluating the neurobehavioral effects of lead exposure using IQ tests is that they may not be the best measure of neurologic dysfunction. Significant, associations between concurrent BPb and visual-motor integration and delayed reaction times at low to moderate levels have been reported.<17,18,20,21> The clinical significance of this finding is unclear and may reflect attentional deficits. While large cross-sectional studies have suggested an association between current BPb levels and stature, the study designs limit their ability to establish a causal relationship. There is fair evidence that prenatal mild and moderate lead exposure does not affect growth, and insufficient evidence to support or refute an adverse effect of postnatal lead exposure on growth. Continued research appears warranted.

Lead and Anemia
Lead exposure also affects red blood cells, typically causing anemia. There have been few reports of anemia due to lead exposure at BPb levels £25 mg/dL.

Maneuver
Most studies of lead effects have used blood lead concentrations as the indicator of lead toxicity, in part because it is a relatively simple and inexpensive test to perform. A single blood lead level cannot distinguish between recent exposure to a high level of lead and chronic exposure resulting in a steady state level.

The precision and reliability of BPb measurements at low and moderate levels may be affected by environmental lead contamination during blood collection and by laboratory analytic variation. Skin lead contamination may also be a problem, particularly with capillary blood sampling. However, studies have demonstrated that adequate attention to methods that minimize the risk of contamination using either capillary or venous sampling results in similar BPb levels.<47-49> Regarding analytic variation, current proficiency testing program criteria for blood lead require that reported results are within ±4 mg/dL of target values for values £40 mg/dL.<50> At BPb levels as low as 10-25 mg/dL, analytic variability of ±4 mg/dL and small errors caused by environmental contamination could lead to inappropriate decisions regarding intervention. Sending a repeat specimen to a different laboratory could increase analytic variation, since between-method variability tends to exceed within-laboratory variability.<1,50,51> Methods for determining BPb have good precision and accuracy but tend to be expensive, cumbersome and relatively slow.<50-52> Among Canadian laboratories specializing in blood lead analysis one would expect at least 10% of the samples to be misclassified if the cutoff point were 10 mg/dL. Changes in BPb levels up to ±8 mg/dL may be due to error and variability.

Erythrocyte Protoporphyrin (EP) measurement is inexpensive, unaffected by environmental lead contamination, is easily performed on capillary blood specimens, and is a better indicator of chronic lead exposure than BPb measurement. However, it appears to lack sensitivity and specificity for lead exposure in the low to moderate range, using BPb as the reference standard.

Inexpensive, non-invasive methods for assessing total body lead burden are clearly needed, particularly for low levels. Until such methods are available, measuring BPb appears to be the best alternative for screening for lead exposure.

Effectiveness of Prevention and Treatment
There have been no controlled trials to demonstrate that routine screening for BPb results in better clinical outcomes than either targeted screening or case-finding, but uncontrolled time series have suggested that screening high-risk populations may be effective in improving clinical outcome when compared to case-finding.<53,54> No controlled trials of targeted screening, and no studies of any kind evaluating universal screening or the health benefits of screening to detect mild or moderate lead exposure, were found in our literature review.

The rationale behind detecting BPb >10 mg/dL is that identification of such levels allows initiation of interventions that will prevent complications of lead toxicity or will prevent subsequent increases in BPb to toxic levels. Controlled trials demonstrating that interventions for persons who have mild to moderate lead exposure produce better outcomes than no intervention have not been reported. Without intervention, mean BPb levels are known to decrease as children age (after a peak at about age 2 years).<12,13> To evaluate adequately the effects of interventions on BPb levels, studies must take into account changes over time, preferably by using untreated controls.

Environmental Lead Abatement
There is good evidence against the use of soil-abatement to reduce BPb levels in children with mild lead exposure, and no evidence concerning clinical benefits of this intervention.<55> There is fair evidence that residential deleading results in significant BPb reductions in children with BPb levels ³25 mg/dL.<56> Data of a beneficial effect on cognitive function of residential deleading with children who have moderately elevated lead levels are limited to a single cohort study.<12> Most studies of residential deleading suffer from important design flaws, particularly the absence of adequate controls and limited follow-up. One-time dust abatement has little effect on BPb in children with mild exposure,<55> but frequent, careful cleaning to reduce lead dust levels appears to cause modest, long-term reductions in BPb levels in children with moderate lead exposure,<57> and is likely to cost substantially less than deleading.

Pharmacologic Intervention
In children with symptomatic, severe lead exposure, treatment with dimercaprol (BAL) plus CaNa2-EDTA appears to reduce morbidity and mortality (Comparisons of times and places, Grade II-3) evidence.<58-64> Treatment of children with severe (³ 55 mg/dL), asymptomatic lead exposure with EDTA or succimer reduces BPb levels to the range where the risk of encephalopathy or death is low, and these effects (at least for EDTA) may be long-lasting (Grade II-3) evidence).<61,65-69>

A large cohort study of EDTA chelation therapy in children aged 13-87 months with BPb levels between 25 and 55 mg/dL<15,70> found no association between chelation and reductions in BPb, bone lead or EP concentration, or improvements in cognitive function. Chelating agents have been associated with short-term reduction in BPb levels in before-after studies,<71-73> but these effects have not been sustained in the absence of other interventions.

Succimer, an oral chelating agent, was approved by the U.S. Food and Drug Administration in 1991 for use in children with BPb levels >45 mg/dL, and appears to have fewer adverse effects than BAL or EDTA. Neither has been evaluated in placebo-controlled trials in children with asymptomatic exposure at levels below 55mg/dl. Penicillamine has been evaluated in two recent retrospective cohort studies of patients with BPb levels 25 to 40 mg/dL<72,73> with encouraging results. However, neither study describes results of long-term follow-up.

No controlled trials evaluating the efficacy or effectiveness of nutritional intervention (such as caloric, calcium or iron supplementation) for children with mild or moderate lead exposure were found.

Adverse Effects of Screening
The adverse effects of venipuncture for initial screening for lead toxicity are minimal, including rare complications of infection or bleeding. Problems may be associated with follow-up findings including financial costs and the inconvenience and anxiety associated with EDTA lead mobilization tests (LMT), although none of these effects have been evaluated in controlled studies. The LMT requires intramuscular or intravenous infusion, a stay at the clinical center for at least 8 hours, and for young children, application of urine collection bags, which are clearly not minor inconveniences. The potential risks associated with EDTA mobilization tests include those of EDTA therapy (see Adverse Effects of Intervention below), which primarily affects renal function. The use of EDTA alone in patients with very high BPb levels has been reported to aggravate neurologic symptoms.<1> However, no evidence of adverse neurologic effects from the current dosage used for the LMT in patients with moderate lead exposure has been reported. A recent study of low income California children revealed that only 0.12% had BPb >25 mg/dl and with a calculated cost of $19,139 to detect each of these children. The 6 children so identified were asymptomatic. Public health resources used to identify these children might have been used more effectively elsewhere.<74>

Adverse Effects of Intervention
For patients identified with lead exposure, interventions in the form of lead abatement or chelation therapy may also produce adverse effects. Residential deleading may result in significant increase in BPb levels during or immediately after the abatement process among resident children and lead abatement workers.<56,75-77> Both EDTA and BAL treatment have substantial toxicity, are invasive (requiring intravenous or intramuscular injection) and generally require hospitalization.<1> Side effects, including mild fever, transient elevations of hepatic transaminase, lacrimation, paresthesias, tachycardia and increases in blood pressure have been reported in 30 to 50% of patients although most side effects are transient. Early case reports of EDTA use at high doses have described acute renal failure and death in a number of patients.<78> Therapeutic EDTA at the lower doses currently used has been reported to cause transient increases in serum creatinine in 13% and reversible oliguric acute renal failure in 3% of 130 children.<79> However, in a series of 608 children treated with EDTA (± penicillamine) over a two year period, only one patient developed proteinuria and edema.<53> EDTA is a non-specific chelator, and has been associated with a 17-fold increase in the daily rate of zinc loss in urine.<80>

The principal adverse effects of d-penicillamine are penicillin-sensitivity- like reactions, such as rashes, leukopenia, and eosinophilia.<53,69,72>

Adverse effects reported in studies of succimer have been uncommon and mild, although clinical experience with this drug is limited compared to other chelators.

Recommendations of Others
The Federal/Provincial Committee on Environmental and Occupational Health is currently finalizing recommendations which will be published in the fall of 1994. The Final Report of The Royal Society of Canada, had the following recommendations: 1) surveys of blood lead levels for the identification of "hot spots"; 2) annual screening during periods of clean-up; and 3) that wherever possible, such surveys be included in surveys undertaken for other purposes. The U.S. Preventive Services Task Force recommendation is currently under review. The U.S. Centers for Disease Control and Prevention (CDC)<1> recommend: 1) universal screening for all children ages 6 months to 6 years, except in communities where it has been demonstrated in large numbers of children (number not specified) that no lead exposure exists; 2) BPb levels beginning at 6 months for children defined as high-risk for high-dose lead exposure based on a brief questionnaire, and at 12-15 months for all other children, with follow-up screening schedules based on risk assessment and previous BPb levels; and 3) that pediatric health-care providers teach parents how to prevent lead exposure, tailoring guidance to likely hazards in the community.

Conclusions and Recommendations
Recent studies suggest that in populations presumed to be at high risk (based on sociodemographics or housing characteristics), the prevalence of mild, moderate, and severe lead exposure is highly variable, with 10-fold differences among different communities. These data suggest a need for each community to conduct its own surveys to determine actual risk. The need for screening is dictated in part by the likelihood of detecting substantial numbers of cases.

A questionnaire developed by the CDC appears to have a sensitivity of 64-87% (based on published studies) for detecting PBb £10 mg/dL, but its sensitivity for detecting moderate or severe lead exposure is unknown and it was not designed as a screening tool. No studies evaluating the CDC or any other questionnaire in a Canadian setting have been reported. Although specificity is poor, use of a validated questionnaire of known and acceptable sensitivity could reduce substantially the number of children requiring screening with BPb to detect those with increased levels.

While there is fair evidence that modest neurobehavioral dysfunction in children is associated with mild to moderate lead exposure as measured by tooth lead levels, the same association with low BPb levels is not clearly established. Since high BPb levels are clearly associated with neurotoxic effects, it is possible that the small effects likely to be seen with mild to moderate BPb exposure are not detectable with current psychometric tests, or that BPb is not a sufficiently accurate measure of lead exposure to detect these effects. Since lead is known to have many toxic effects, it may have effects at low levels, although the clinical importance of such effect sizes for the individual is questionable. On a population basis however, the cumulative effects of small reductions in IQ might be substantial.

For moderate lead exposure (25-49 mg/dL), no association was found between chelation with EDTA and improvements in IQ, and other interventions have not been evaluated with regard to morbidity. Scientific studies of adequate quality evaluating the ability of chelation or residential deleading to produce sustained reductions in moderately elevated BPb levels appear to have given equivocal results. In the experimental setting, twice monthly dust abatement by a research assistant has shown modest long-term reductions of moderately elevated (30-50 mg/dL) BPb levels, although the effectiveness of counselling families to provide this intervention in their homes has not been evaluated.

We found no studies that evaluated the effectiveness of early detection of mild lead exposure in improving clinical outcomes. Good evidence from a randomized controlled trial showed little effect on low BPb levels from either soil abatement or one-time interior dust abatement. Adequate studies evaluating chelation, residential deleading or other interventions, such as nutrition counselling, for mild lead exposure have not been reported.

One might argue that results from studies at high levels should be extrapolated to lower levels. However, the available evidence shows little or no benefit from intervention at low to moderate levels. In addition, there are important risks associated with such interventions, including substantial increases in BPb levels with residential deleading, and the potential for adverse effects from chelation therapy.

Given the low prevalence of elevated BPb levels in the general Canadian population, the relatively small burden of suffering from low to moderate lead exposure, and the limited data demonstrating the effectiveness of intervention, there is currently insufficient evidence to recommend for or against universal BPb screening of children to detect mild or moderate lead exposure (C Recommendation).

On the other hand, there are children who are at high risk for severe lead exposure either because of individual risk factors or because the prevalence in their community is high. These children may already be at increased risk for neurobehavioral dysfunction because of poverty, malnutrition, etc., and are more likely to have BPb levels in the range for which intervention has shown some effectiveness. They are therefore more likely to benefit from screening for lead toxicity (B Recommendation). In communities known to have very high prevalences of lead exposure (e.g., in certain inner cities, or near lead smelters), targeted screening may be more efficient and is most sensitive.

Clinical Intervention
Children found to have BPb ³50 mg/dL should be treated according to current standards for chelation and/or environmental deleading. There is currently insufficient evidence to recommend for or against chelation therapy or residential deleading as a preventive maneuver for children with blood lead levels 10-49 mg/dL. Soil abatement and one-time household dust abatement are not recommended for the households of children with BPb levels £20 mg/dL.

For primary prevention of lead exposure, clinicians should consider informing families living in homes built before 1950, especially those in deteriorated condition, of the potential benefits of regular cleaning to reduce lead dust, including twice monthly wet-mopping with a high-phosphate detergent cleanser of all surfaces containing (or presumed to contain) high lead levels.

Unanswered Questions (Research Agenda)
The following have been identified as research priorities:

1. Evaluation of the many other contributors to neurologic dysfunction that may interact with lead, such as nutritional factors, genetic susceptibilities, and other toxins (including cigarettes and alcohol).
2. Evaluation of the ability of residential abatement, oral chelation therapy, nutritional interventions, and physician counselling to reduce low to moderate BPb levels, especially on a long-term basis.
3. Determination of the long-term effects on neurobehavioral dysfunction of reducing low to moderate lead levels.
4. Validation of questionnaires to screen for children at increased risk of lead exposure, particularly in rural and minority populations.

Acknowledgements
The Task Force thanks Sarah Shea, MD, FRCP, Assistant Professor, Department of Pediatrics, Dalhousie University, Halifax, NS, for reviewing the draft report.

Full Citation
Feldman, W. & Randel, P. Screening children for lead exposure in Canada. In: Canadian Task Force on the Periodic Health Examination. Canadian Guide to Clinical Preventive Health Care. Ottawa: Health Canada, 1994; 268-288.