DoctorFinder | Join/Renew | MyAMA | Site Map | Contact Us

Lead poisoning among children

Note: This report represents the medical/scientific literature and AMA policy on this subject as of December 1994.

Full text

Over the last few years, increasing concern has been expressed about the effect of lead on the development and neurological functioning of children. Federal programs have called for more aggressive screening and lead removal activities by public and private entities. AMA policy has supported alerting the public to the danger of lead-based paint (Policy H-440.943,  AMA Policy Compendium) and has supported the development of standards to achieve non-hazardous levels of exposure to lead and other metals arising from common household and workplace products (Policy H-135.959). The AMA has also expressed concern about the specific recommendations and implications of the Centers for Disease Control and Prevention (CDC) program to augment childhood blood lead screening (Policy H-60.968). This report examines issues relevant to the clinical effects of lead, treatment of elevated blood lead concentrations, and policy issues concerning lead screening and prevention.

Introduction

Children are exposed to lead from a number of sources, including leaded paint, dust, soil, water, air, and food. Lead contamination from bullet fragments that cannot be removed has also been reported.1 Ingestion of particles from lead-based paint continues to be the most concentrated source of lead exposure for children.2 Over the past 15 years, there have been major reductions in air-borne lead and lead in food.3 These reductions have occurred through the phasing out of leaded gasoline and the elimination of cans with lead-soldered seams. The exception to the latter is some imported food, which continues to be packaged in cans with lead seams. 

Average blood lead concentrations have declined dramatically. About 25 years ago, the average blood lead concentration in the United States was 16 µg/dL.4 Data from the National Health and Nutrition Examination Surveys II and III (phase 1) indicate that the overall mean blood level for the United States has declined to 2.8 µg/dL.5,6

Despite these gains, lead poisoning continues to be a common problem among young children in the United States.3,6 It is currently estimated that 8.9 percent of children between the ages of one and five have a blood lead level equal to or greater than 10 µ/dL.5 Because of developmental factors, children are at a substantially higher risk than adults of lead poisoning. Consequently, most governmental public health efforts have focused on lead poisoning prevention among children.

In 1988, the Agency for Toxic Substance and Disease Registry (ATSDR) estimated that millions of children in the United States continued to have elevated blood lead levels, across all geographic and socioeconomic strata.7 Minority children living in the inner cities are particularly vulnerable, due to lead-based paint in older, deteriorating housing, lead particles from automobile exhaust, industrial pollutants in urban neighborhoods, and parents working in lead containing occupations. African-American children living in poverty have been estimated to have the highest prevalence of elevated lead levels.8 It is estimated that 21 percent of non-Hispanic black American children under six have a blood lead level greater than or equal to 10 µg/dL.6

History

Most European countries signed a treaty in 1921 banning the use of lead-based paint in building interiors. In contrast, the United States took little action until the late 1960s, when the first federal laws were enacted that mandated states to establish lead screening and lead abatement programs. The Lead-Based Paint Poisoning Prevention Act of 1971 authorized screening and treatment programs, removal of lead-based paint from federally-assisted homes, and prohibition of lead-based paint in areas thought to be accessible to children.9

Until 1970, blood lead levels less than 60 µg/dL were considered to be acceptable. In 1970, the Surgeon General of the United States reset the toxicity definition at 40 µg/dL. In 1978 the CDC lowered this index to 30, and then to 25 in 1985. In 1991, the index of toxicity was again lowered to 10 µg/dL. 

Epidemiology

In the U.S., 1.7 million children under six are estimated to have blood lead levels at or above 10 ìg/dl.10 An elevated blood lead level is defined as a level high enough to require medical evaluation for the possibility of adverse mental, behavioral, physical, or biochemical effects.11

In 1988, the ATSDR issued a report to Congress entitled, "The Nature and Extent of Lead Poisoning in Children in the United States."12 That report estimated that 13.6 million U.S. children under age seven potentially were being exposed to lead paint in concentrations high enough to cause adverse effects. The report also estimated that between 5.9 and 11.7 million U.S. children were exposed to dangerously high levels of lead in soil and dust at that time. Furthermore, an estimated 6.6 million children under the age of 14 were exposed to lead in tap water (from old lead pipes or lead soldering in new plumbing). It was the estimate of the ATSDR that 241,000 children under six had blood lead levels greater than 15 µg/dL as a result of drinking contaminated water.

Characteristics that affect an individual's vulnerability to lead include genetics, nutritional status, behavior, and age.11 Children under age six are particularly vulnerable to the effects of lead. Although elevated blood lead levels are found in children of all races and socioeconomic standing, black, poor, and inner-city children are at greatest risk.5,6,13

Excess lead exposure has also been associated with such demographic factors as large family size, number of preschool children in the family, deteriorated housing, low socioeconomic status, marital separation of parents, unemployment of parents, lack of day care facilities, and poor prenatal nutrition.11,14 Certain immigrant populations (Mexican, Hmong, and Asian Indian) can be at risk through lead-containing folk remedies, pottery, and glassware. 15-18

Trend data from the National Health and Nutrition Examination Survey (NHANES II 1976-80) indicate that mean blood lead levels have decreased among U.S. children. This decline has been closely correlated with reduced lead content in gasoline. At the same time, however, recent evidence suggests that blood lead levels previously thought to be safe can result in adverse effects.13 The net result is that the total number of children considered at risk of adverse effects has increased in recent years.19,20

When the CDC revised its 1985 toxicity criterion downward to 10 µg/dL,21 the new definition designated an extraordinary number of children at neurotoxic risk.12 Using the new definition of lead toxicity, it has been estimated that 8.9 percent of U.S. children under six have blood lead levels in the toxic range.7

Federal policy 

In 1991, the Assistant Secretary for Health for the Department of Health and Human Services (DHHS) unveiled a plan to eradicate childhood lead poisoning, entitled "The Strategic Plan for the Elimination of Childhood Lead Poisoning." The stated goal of the strategic plan is to eliminate childhood lead poisoning as a public health problem in 20 years. It calls for an initial focus on children with blood lead levels of 25 µg/dL or more. The four immediate elements of the plan are:

  1. Increased screening of children for elevated blood levels, together with community prevention programs; 
  2. Elimination of leaded paint and paint-contaminated dust hazards in high-risk housing; 
  3. Continued reduction of children's exposure to other sources of lead in the environment; and 
  4. Establishment of national surveillance for children with elevated blood levels, making elevated blood lead levels the first reportable environmental disease.21

Legislation is also pending to mandate medical surveillance by the Occupational Health and Safety Administration (OSHA) for lead workers in the construction industry. 

Implementing this federal strategy will be an expensive undertaking. However, estimates are that averted costs will compensate for the necessary expenditures.3 The CDC estimated the savings in medical costs from preventing a child's blood lead level from reaching 25 µg/dL at $1300. The savings in special education costs per child are $3331. Using these and other data, they estimated the total benefits for abatement of a single dwelling over its lifetime to be $4323 per unit. The net benefit in dollars gained over cost from abatement exceeds $2000 per unit abated.3

In 1992 the Health Care Financing Administration began requiring virtually all young children on Medicaid to be screened (both verbally and by blood test) for lead poisoning. As a result, it is likely that greater numbers of children will be referred for environmental and medical treatment. 

Federal costs attached to the lead prevention effort are considerable. Agencies directly involved include the Department of Housing and Urban Development (HUD), the Environmental Protection Agency (EPA), the Food and Drug Administration (FDA), OSHA, and CDC. The CDC has estimated that implementation of the first five years of the DHHS strategy will cost $974,000,000.22

The EPA has published a strategy for reducing lead in soil, water, air, and various commercial products. The FDA has prepared regulations designed to eliminate all remaining uses of lead-soldered cans in the United States and to set levels of lead considered to be acceptable for wine. Likewise, OSHA is in the process of revising its standards for occupational exposure to lead.23

HUD has requested $25,000,000 annually for four years to assist low- and moderate-income homeowners with lead abatement. It has also made ten grants to cities and states to study cost effective strategies for lead abatement.

Finally, CDC was funded at $7,900,000 for 1991 and was budgeted for $15,000,000 in 1992. These monies go to underwrite screening programs and to support communities with follow-up environmental services.

Clinical and social implications

On entering the body, lead is carried by the blood stream into both soft and hard tissue.24 Blood-lead content is generally considered to be the most accurate measure of short-term lead exposure. While about 50 to 60 percent of the lead entering a person's body is eliminated fairly rapidly,6 most of the remainder is stored in bone, where it has an estimated half life of about 20 years.25 Previously thought to be inert, bone-based lead is now considered a significant threat to the body. Many conditions can lead to the rapid remobilization of bone-based lead, including pregnancy and osteoporosis.26

There is growing evidence that relatively low levels of blood lead can produce verbal, perceptual, motor, and behavioral disabilities in children.27-29 These effects can include hearing impairment, irritability, delayed physical development, inattentiveness, inability to follow instructions, and lowered test scores for reading, spelling and IQ.27-36 Blood lead levels as low as 10 µg/dL have been associated with decreased intelligence and impaired neurobehavioral development.27-29,36-38

The concern about adverse effects of blood lead levels as low as 10 µ/dL is based on a number of epidemiologic and experimental studies.3,21,37,38 Inconsistencies have been found in the results of these studies. However, the weight of the evidence supports the hypothesis that negative effects on cognition are evident at blood lead levels below 25 µg/dL. A recent statement by the American Academy of Pediatrics (AAP) notes that a decrease of four to seven IQ points has been associated with every 10 µg/dL increase in blood lead levels.39

One recent study40 suggests that the decline in intelligence caused by accumulated lead can be at least partially reversed when steps are taken to reduce blood levels. The study found that decreased blood lead levels were associated with cognitive improvement among children with moderate lead poisoning. The researchers concluded that the standardized test scores of children ages one to six improved by one point for every 3 µg/dL decrease in their blood lead level. Significantly, this improvement was not found to be related to chelation specifically.

Fetal exposure to lead is measured from umbilical cord blood. Maternal and cord blood lead levels of 10-15 µg/dL appear to be associated with reduced gestational age and reduced birth weight.12,29 Prenatal lead exposure has been associated with minor physical anomalies and growth deficits in neonates.10,11,30,41,42 There is a negative association between cord blood lead levels and early childhood cognitive functions, an effect that may no longer be clinically or statistically significant by the time the child enters school.

At high blood concentrations, many organs and systems are affected by lead, including the kidneys, liver, gastrointestinal tract, myocardium, immune system, reproductive system, and central and peripheral nervous systems.10 When blood lead levels in young children exceed 60 µg/dL, the risk for acute encephalopathy dramatically increases.3 Without medical intervention, encephalopathy may evolve quickly over a course of days, from mild lethargy, ataxia, and confusion to coma, convulsions, and severe brain edema. At this stage, children can die from complications of increased intracranial pressure. Survivors are often left with major intellectual and behavioral disorders.43

Prevention and treatment 

Prevention activities and national surveillance are essential to eliminating lead poisoning in children. Massachusetts has the highest statewide screening penetration in the nation--40 percent in 1986. In high-risk urban areas, their screening penetration reached 72 percent. Between 1985 and 1986, the number of new cases of lead poisoning in Massachusetts dropped 30 percent. Nevertheless, more than 1,000 Massachusetts children suffered from lead poisoning in 1986, a number state officials labeled "unacceptably high for a preventable disease."44

Screening is essential so that affected children can receive appropriate medical attention and environmental follow-up. This is particularly true in geographic areas known to have a high prevalence of children with seriously elevated blood lead levels. Surveillance data can be used to identify those areas in greatest need of intensive abatement programs, as well as to evaluate the success of the national abatement program.2 Some scientists have questioned the cost-benefit ratio of universal vs. targeted screening. They take the position that targeted screening is appropriate in geographic areas known to have a low incidence of elevated blood lead levels.45 The 1991 CDC guidelines called for virtually universal screening, except in communities with a low prevalence of elevated blood lead levels among children. However, these guidelines did not provide explicit criteria for defining "communities with a low prevalence." The CDC is currently developing data that will allow them to define more clearly the circumstances under which a shift to targeted screening would be appropriate.

The blood lead level determines the type of treatment necessary. Potential interventions include frequent rescreening, parent education, environmental investigation and clean-up, testing other children potentially exposed, medical evaluation, and chelation therapy. For any affected child, the primary goal is to eliminate future exposure through hazard abatement.46 Collateral goals are to reduce susceptibility through improved nutrition and reduce lead burden through intravenous or oral chelation therapy.21

Abatement: There are two types of lead hazard control measures. Interim controls temporarily reduce exposure, while abatement permanently eliminates or renders inaccessible sources of lead hazard. Interim controls include specialized cleaning, repairs, maintenance, painting, sealing of floors and other porous surfaces, temporary containment, management, and resident education programs.

Hazard abatement is an integral part of both treatment and prevention. Lead-based paint and paint-contaminated house dust are still the major causes of high-dose lead poisoning in U.S. children. The greatest concentrations of leaded paint occur in housing built before 1950. The success of abatement programs hinges on a coordinated effort from the public and private sectors. Leaded paint abatement is difficult, potentially dangerous, and expensive.

At present, there are four accepted strategies for lead abatement--replacement of building components, enclosure, encapsulation, and paint removal. Of the three, paint removal is the least desirable because of the leaded dust generated, and it can be costly when done properly. In replacement, building components such as woodwork, windows, trim, frames, doors, and moldings are carefully removed. New or de-leaded components are then installed in their place. In some cases, larger woodwork is removed, inverted, reinstalled, and then sealed. Enclosure involves covering potential surfaces with a rigid or semi-rigid material that is attached to the building structure. Examples include gypsum board, vinyl siding, and plywood.

According to HUD, encapsulation involves coating or sealing leaded surfaces with materials that are specially formulated to be elastic, durable, and resistant to cracking, peeling, vermin, fire, and fungi. Paint, wallpaper, and contact paper are not considered to be acceptable encapsulants. Examples of acceptable materials include such things as gypsum board, aluminum, formica, fiberglass, plywood, vinyl, and durable wall-to-wall carpeting. Encapsulation is the recommended method for dealing with large surfaces that cannot be replaced (such as walls).

There are on-site and off-site approaches to paint removal. Of the two, off-site is more desirable as it creates less leaded waste and fumes. Removal of leaded paint should only be done by contractors with special training in lead abatement, as it is exacting and dangerous work. When a residence is undergoing abatement, all family members should be quartered elsewhere until the work has been completed.

There has also been some experimentation with abatement of soil-based lead through removal and replacement. A recent study concludes that this approach does not have sufficient effect to be clinically useful.47 Soil remediation (by covering with foliage or pavement) may be an alternative.46

Chelation therapy: Most experts agree that chelation therapy is not recommended for children with lead levels below 25 µg/dL. The most common practice is to chelate children with levels of 45 µg/dL or above. Chelation has been shown to reduce blood lead levels, but there are little data on its relationship to the prevention or improvement of cognitive delay. 

Chelation therapy cannot serve as a substitute for removing the child from the source of lead exposure. In fact, chelation therapy done while the child remains in a lead-containing environment can be dangerous, as the treatment can enhance the intestinal absorption of lead. 

Chelation therapy lowers blood lead and mobilizes lead stored in skeletal tissue. It is not yet known whether chelation can mobilize and remove lead from brain tissue. Four chelating agents are currently available--CaNa2EDTA, BAL, D-penicillamine, and succimer. D-penicillamine is not approved by the FDA for treating lead poisoning. Chelating agents facilitate the urinary excretion of lead but may deplete other essential metals, such as calcium, magnesium, iron, and zinc. The loss of these essential metals is responsible for some of the attendant risks of chelation. Notable side effects include transient transaminase elevations, gastrointestinal upset, headaches, hypersensitivity reactions, renal damage, transient neutropenia, and mild conjunctivitis.48

Intravenous chelation therapy can be expensive. Associated costs include hospitalization, laboratory services, physician visits, and psychological testing. Outpatient treatment is becoming more common, but is also expensive.

Testing

Even careful history-taking can miss many common sources of lead exposure. Consequently, the major approach to lead screening in children is blood testing. Historically, physicians have used the erythrocyte protoporphyrin (EP) test as a lead screening tool. This test does not directly measure blood lead levels. Rather, it is an index of heme synthesis. Impaired heme synthesis is one of the biochemical effects of lead toxicity. EP tests can be elevated for several reasons, however, including iron deficiency anemia. Further, EP testing is not acceptably sensitive to elevated lead levels, particularly those less than 25 µg/dL.49

The major argument for universal screening is to identify and properly manage children at risk for lead poisoning. However, there is some disagreement about the cost-effectiveness of universal screening.45,50 Proponents of universal screening cite the need to accumulate reliable surveillance data about the levels of lead exposure in various communities. They argue that only after a community has been shown to have minimal numbers of lead-affected children can selective screening based on risk be considered. The CDC,21 AAP,39 and most experts now recommend screening all children by direct testing of blood lead levels. Using venous blood samples is the most reliable approach. However, the issue of practicality often leads to blood lead screening by capillary sample.51 These results can be quite specific and accurate, but are vulnerable to contamination by lead on the child's skin. Proper finger cleaning prior to obtaining the sample is effective, but any significant elevation found on a capillary sample should be confirmed through a venous blood test. 

In their recently updated statement,39 the AAP recommends that pediatric providers screen for lead exposure both verbally and through blood lead screening. AAP recommendations call for universal screening of children between nine and 12 months of age and, if possible, again at about two years of age. They also call for regular verbal screening of lead risk at each health visit between the ages of six months and six years of age. 

Certain clinical conditions also should alert physicians to possible lead toxicity. These include growth failure, speech and developmental disorders, hyperactivity, unexplained seizures, neurologic symptoms, abdominal pain, and hearing loss. 

Management of children with elevated blood lead levels

Treatment and management approaches vary. The following approaches are common, however:

Blood lead levels  < 9 µg/dL

Continue verbal screening at scheduled visits

Re-test following universal protocol or if identified risk increases

No treatment required

Blood lead level 10-14 µg/dL

Age 6 - 36 months, retest in four months

Age 37 - 72 months, retest in a year

Conduct environmental investigation

Provide environmental remediation of identified sources if resources allow

Give health education to parents

Assess nutritional status and correct any identified deficiencies

Blood lead level 15-24 µg/dL

Retest every three to four months

Conduct environmental investigation and provide environmental remediation

Conduct a complete medial evaluation, with special attention to assessing nutritional status

Give health education to parents

Consider testing other potentially exposed children (e.g., siblings or fellow day-care recipients)

Blood lead level 25-44 µg/dL 

Retest to confirm results

Consider the appropriateness of chelation therapy

Conduct environmental investigation and provide environmental remediation

Conduct a complete medical evaluation, with special attention to assessing nutritional status

Give health education to parents

Test other potentially exposed children

Blood lead level  > 45 µg/dL

Retest immediately to confirm results

If confirmed, provide chelation therapy

Conduct environmental investigation and provide environmental remediation

Conduct a complete medical evaluation, with special attention to nutritional status

Base further treatment decisions on the results of blood lead level obtained over time 

Test other potentially exposed children

Role of physicians

It is essential that physicians participate in preventing and eliminating childhood lead poisoning. Important physician contributions include providing anticipatory guidance to parents, verbal screening of children and parents about potential sources of lead exposure, testing and interpreting blood lead levels, case coordination to ensure that affected children receive appropriate medical, social, and environmental services, and working with public health officials. A recent study has documented a high frequency of "missed opportunities" for lead screening during unrelated medical visits.52

Parental education: Physicians should discuss with parents the potential hazards of lead. These discussions should focus on the major preventable sources of high-dose lead poisoning, including lead-based paint and take-home exposure from parents' occupations and hobbies. Specific attention should be given to the potential dangers of peeling paint, the potential hazards of renovating older homes, and the need for good work practices when occupations or hobbies involve exposure to lead.21 Other educational efforts should be tailored to likely exposures in the community.

Coordination: Physicians also must support state and local efforts to control lead hazards. Private physicians and public health agencies can cooperate to eliminate childhood lead poisoning. Private physicians should report cases of elevated lead levels to their local health departments. In return, public officials can be an important source of information about the extent of the lead poisoning problem in the community and particular lead sources that may be of concern in a given neighborhood. Often these officials can also assist in the management of the lead-poisoned child, including follow-up screening, environmental investigations, and lead hazard abatement. 

Summary

Lead poisoning continues to be a common and significant environmental threat to young children. In the United States today, between one and two million children from all geographic areas and socioeconomic strata have lead levels high enough to cause adverse health affects. Poor, minority children in the inner cities are at particular risk. 

In 1991 the federal government released a strategic plan that outlined the first five years of a 20-year effort to eliminate childhood lead poisoning as a public health problem. The plan encompasses both a research and a programmatic agenda. Cooperative efforts between DHHS, EPA, HUD, and state and local programs are essential to the success of this plan. 

Childhood lead exposure costs the United States billions of dollars in medical and special education costs and decreased future earnings. Most exposures occur in the home, with lead-based paint continuing to be the principal high-dose source. 

While progress has been made, continued need exists for efforts to prevent lead poisoning among children. Doing so will require effort by many groups, including public health officials, environmental agencies, housing agencies, and health care professionals. Appropriate screening programs will be essential to the effort. 

Physicians can play a critical role in preventing lead poisoning, both in their practices and by governmental advocacy. It is important that the tradition of public involvement continue and that physicians continue to act publicly as advocates for the health of children. 

Recommendations

The following statements, recommended by the Council of Scientific Affairs, were adopted by the AMA House of Delegates as AMA policy at the 1994 AMA Interim Meeting.

The AMA:

  1. Encourages physicians and public health departments to regularly screen all children under the age of six for lead exposure through history-taking and when appropriate by blood lead testing. The decision to employ blood testing should be made based on prevalence studies of blood levels in the local pediatric population. Findings from these studies will determine whether universal or targeted screening should be employed; and  
  2. Encourages the reporting of all children with elevated blood levels to the appropriate health department in their state or community. In some cases this will be done by the physician, and in other communities by the laboratories.

References

  1. Kikano GE, Strange KC. Lead poisoning in a child after a gunshot injury.  J Fam Pract. 1992;34:498, 500, 502, 504.  
  2. Fee E. Public Health in Practice: An Early Confrontation with the 'Silent Epidemic' of childhood lead poisoning.  J Hist Med Allied Science. 1990;45:570-606.  
  3. Centers for Disease Control and Prevention. Strategic Plan for the Elimination of Childhood Lead Poisoning. Atlanta: US Department of Health and Human Services, Public Health and Human Service, 1991.  
  4. Mahaffey KR, Annest JL, Roberts J, Murphy RS. National estimates of blood lead levels: United States, 1976-1980: association with selected demographic and socioeconomic factors.  NEJM   1983;308:1373-1377.  
  5. Brody DJ, Pirkle JL, Kramer RA, Flegal KM, Matte TE, Gunter EW, Paschal DC. Blood lead levels in the US population. Phase 1 of the Third National Health and Nutrition Examination Survey (NHANES III, 1988 to 1991),  JAMA. 1994;272:277-283.  
  6. Pirkle JL, Brody DJ, Gunter EW, Kramer RA, Paschal DC, Flegal KM, Matte TD. The decline in blood lead levels in the United States. The National Health and Nutrition Examination Surveys (NHANES).  JAMA. 1994;272:284-291.  
  7. US Department of Health and Human Services. Public Health Service. A Public Health Service Progress Report on Health. People 2000: Environmental Health. Washington, DC: US Department of Health and Human Services, 1992.  
  8. Needleman HL, Jackson RJ. Lead toxicity in the 21st century: will we still be treating it?  Pediatrics. 1992;89:678-680.  
  9. 42 USC Sections 4801-4846.  
  10. Mushak P, Crocetti A. Testimony before the Subcommittee on Health and Environment, Committee on Energy and Commerce, U.S. House of Representatives, 10 Dec 1987, University of North Carolina and New York Medical College. Washington D.C., 1987.  
  11. Needleman H, Bellinger D. The developmental consequences of childhood exposure to lead: recent studies and methodological issues.  Adv Clin Child Psychol. 1984;7:195-220.  
  12. Agency for Toxic Substances and Disease Registry. The Nature and Extent of Lead Poisoning in Children in the United States: A Report to Congress. Atlanta: US Dept of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry, 1988.  
  13. Miller CA, Fine A, Adams-Taylor S. Monitoring Children's Health, 2nd ed. Washington, D.C.: American Public Health Association, 1989.  
  14. Lin-Fu J. Children and lead: new findings and concerns.  NEJM. 1982;307:615-617.  
  15. Centers for Disease Control and Prevention. Use of lead tetroxide as a folk remedy for gastrointestinal illness.  MMWR. 1981;30:456-457.  
  16. Centers for Disease and Prevention. Folk remedy-associated lead poisoning in Hmong children--Minnesota.  MMWR. 1983;32:555-556.  
  17. Centers for Disease Control and Prevention. Lead-poisoning-associated deaths from Asian Indian folk remedies--Florida.  MMWR. 1984;33:638-645.  
  18. Lead poisoning associated with use of traditional ethnic remedies--California, 1991-1992.  MMWR. 1993;42:421-424.  
  19. Centers for Disease Control and Prevention. Childhood lead poisoning-United States: Report to Congress by the Agency for Toxic Substances and Disease Registry.  MMWR. 1988;37:481-485.  
  20. Annest J, Mahaffey K Cox D, Roberts J. Blood lead levels for persons 6 months-74 years of age: United States, 1976-1980. Washington, D.C.: National Center for Health Statistics, 1982.  
  21. Centers for Disease Control and Prevention. Preventing lead poisoning in young children: a statement by the Centers. Atlanta: Centers for Disease Control, 1991.  
  22. Mason JO. From the Assistant Secretary for Health, US Public Health Service.  JAMA. 1991;265:2049.  
  23. Adult blood lead epidemiology and surveillance.  MMWR. 1993;42:84-85.  
  24. Rabinowitz MB, Wetherill TW, Kopple JD. Kinetic analysis of lead metabolism in healthy humans.  J Clin Investigations. 1976;58:260-270.  
  25. Zylke JW. Preventive medicine's latest goal: getting lead out to protect children.  JAMA. 1991;266:315-316.  
  26. Silbergeld EK, Schwartz J, Mahaffey K. Lead and osteoporosis: Mobilization of lead from bone in menopausal women.  Environ Res. 1988;47:79-94.  
  27. Mushak P, Davis JM, Crocetti AF, Grant LD. Prenatal and postnatal effects of low-level lead exposure: Integrated summary of a report to the US Congress on childhood lead exposure. Environ Res. 1989;50:11-36.  
  28. Schonfeld DJ. New developments in pediatric lead poisoning. Current Opinion in  Pediatrics 1993;5:537-544.  
  29. Dietrich KN, Berger OG, Succop PA, Hammond PB, Bornschein RL. The developmental consequences of low to moderate prenatal and postnatal lead exposure: Intellectual attainment in the Cincinnati lead study cohort following school entry.  Neurotocol Teratol 1993;15:37-44.  
  30. Davis J, Svendsgaard D. Lead and child development.  Nature. 1987;329:297-300.  
  31. Lin-Fu J. Vulnerability of children to lead exposure and toxicity.  NEJM. 1973;289:1229-1233,1289-1293.  
  32. Mahaffey K, Annest L, Roberts J, Murphy R. National estimates of blood lead levels: United States 1976-1980.  NEJM. 1982;307:573-579.  
  33. Needleman H, Gunnoe C, Leviton A, Reed R, Deresie H, Maher C, Barrett P. Deficits in psychologic and classroom performance of children with elevated dentine lead levels.  NEJM. 1979;300:689-695.  
  34. Bellinger D., Needleman HL, Bromfield R, Montz M. A follow-up study of the academic attainment and classroom behavior of children with elevated dentine lead levels.  Biological Trace Element Research. 1984;6:207-223.  
  35. Schwartz J, Angle C, Pitcher H. Relationship between childhood lead levels and stature.  Pediatrics. 1986;77:281-288.  
  36. Schwartz J, Otto D. Blood lead, hearing thresholds, and neurological development in children and youth.  Arch Env Health. 1987;42:153-160.  
  37. McMichael AJ, Baghurst PA, Vimpani GV, Wigg NR, Robertson EF, Tong S. Tooth lead levels and IQ in school-age children: The Port Pirie cohort study.  Am J Epidemiol 1994;6:489-499.  
  38. Bellinger DC, Stiles KM, Needleman HL. Low-level lead exposure, intelligence, and academic achievement: A long-term follow-up study.  Pediatrics 1992;90:855-861.  
  39. AAP Committee on Environmental Health. Lead poisoning: from screening to primary prevention.  Pediatrics. 1993;92:176-183.  
  40. Ruff HA, Bijur PE, Markowitz M, Ma Y, Rosen JF. Declining   blood lead levels and cognitive changes in moderately lead-poisoned children. JAMA. 1993;269:1641-1646  
  41. Bellinger D, Leviton A, Waternaux C, Needleman HL, Rabinowitz M. Longitudinal analyses of prenatal and postnatal lead exposure and early cognitive development.  NEJM. 1987;316:1037-1043.  
  42. Mushak P, Crocetti A. The Nature and Extent of Lead Poisoning in Children in the United States: A Report to Congress. Atlanta: Agency for Toxic Substances and Disease Registry, U.S. Public Health Service, 1988.  
  43. Goldstein GW. Nuerologic concepts of lead poisoning in children.  Ped Anns. 1992;21:384-388.  
  44. National Coalition on Prevention of Mental Retardation. The Massachusetts lead program: moving toward Phase 2. Prevention Update 1987. Washington DC: National Coalition on Prevention of Mental Retardation, 1987.  
  45. Harvey B. Should blood lead screening recommendations be revised?  Pediatrics. 1994;93:201-204.  
  46. Binder S, Matte T. Childhood lead poisoning. The impact of prevention.  JAMA. 1993;269:1679-1681.  
  47. Weitzman M, Aschengrau A, Bellinger D, Jones R, Hamlin JS, Beiser A. Lead-contaminated soil abatement and urban children's blood lead levels.  JAMA. 1993;269:1647-1654.  
  48. Drug Evaluations Annual, 1993. Chicago: American Medical Association, 1993.  
  49. Chao J, Kikano GE. Lead poisoning in children.  Am Fam Physician. 1993;47: 113-120.  
  50. Gellert GA, Wagner GA, Maxwell RM, Moore D, Foster L. Lead poisoning among low-income children in Orange County, California. A need for regionally differentiated policy.  JAMA. 1993;270:69-71.  
  51. Schonfeld DJ, Cullen MR, Rainey PM, Berg AT, Brown DR, Hogan JC, Turk DS, Rude CS, Cicchetti DV. Screening for lead poisoning in an urban pediatric clinic using samples obtained by fingerstick.  Pediatrics 1994;94:174-179.  
  52. Campbell JR, McConnochie KM, Weitzman M. Lead screening among high-risk urban children. Are the 1991 Centers for Disease Control and Prevention guidelines feasible?  Arch Pediatr Adolesc Med. 1994;148:688-693.

Reports by topic

Last updated: Sep 24, 2007
Content provided by: CSAPH