Linda George, MD
Kaedrea Jackson, MD
Robert J. Karp, MD
SUNY-Downstate Medical Center
Brooklyn, NY
Pre-test
Q1. T or F. There is no threshold for lead effects and thus no safe blood lead level.
Q2. T or F. Once exposure of lead is resolved, the child is cured.
Q3. T or F. According to local law, it is the parent's responsibility to remove lead based paint from a rented apartment.
Q4. Best answer: At what BLL (?g/dL) should you consider chelation therapy?
A. >20
B. >25
C. >45
D. >70
Objectives
On completion of this module, residents and physicians will be able to:
1. Appreciate the use of lead throughout history.
2. Recognize and understand the consequences associated with lead exposure
3. Identify the role of lead as an "anti-nutrient".
4. Appropriately manage patients exposed to lead.
Facilitator preparation
The following material is suggested for review:
American Academy of Pediatrics. Committee on Environmental Health Screening for Elevated Lead Blood Levels. Pediatrics. 1998; :1072-1078
American Academy of Pediatrics Committee on Environmental Health Lead Exposure in Children: Prevention, Detection, and Management
Pediatrics 2005;116 4):1036-1046
Lanphear BP, Homoung R, Khory J, et al, Low-level environmental lead exposure and children's intellectual function: an international pooled analysis. Environ Health Perspect. 2005 Jul;113(7):894-9.
This module is based in part on
Karp RJ. Calder L. (1996) Lead & Nutrition. A monograph prepared for the New York State Department of Health. (and)
Harris P, Clark M, Karp RJ. (1993) The prevention of lead poisoning
(in) Karp RJ (ed) Malnourished Children in the United States: Caught in the Cycle of Poverty. Springer Publishing Co of New York
Introduction
Lead is a divalent cation, which in lay terms would be considered an anti-nutrient. Because of its structure and charge, lead engages in reactions and is substituted for the essential nutrients calcium, iron and zinc. Lead when absorbed in the body is stored in cartilage, bones and teeth. It affects neurological development and is associated with anemia and growth failure.
Investigation of the consequences of lead poisoning in childhood have been hindered by its occurrence in disadvantaged populations where the cluster affect of poverty are likely to obstruct the identification of specific causes. Studies of industrial exposure among children from the breadth of socioeconomic background, however confirm the most significant consequence-developmental delay with low lead exposure in utero and in early life. Mouthing behavior is normal for children under 18 months of age. Thus, with exposure, lead poisoning of small children is inevitable and is without regard to the educational achievement, social, or economic status or parenting ability of the family.
History
For several thousand years, humankind has been able to extract and process metals from the ground for everyday use. The use of lead piping for water and lead-based piping for drinking are thought to have caused mass poisoning of Roman populations. In preindustrial societies (as in Mexico today), poorly fixed lead based glazing of pottery has been a cause for poisoning. Inks containing lead exposed printers to lead poisoning early in the development of printing. Benjamin Franklin recommended that zinc replace lead in printer's ink. By the early 20th century, the major contributors to industrial exposure have been identified. These include exposure to lead in the production of paint, storage batteries, pottery, and manufacture of solder and brass.
More recently, lead became common additive to gasoline affecting both workers in the refineries and. those exposed to the exhaust of automobiles. In our own inner-city communities, the principal concern is deteriorating housing with lead based pint and plaster dust and debris peeling off walls and ceilings in the path of small children. A contemporary concern has been the high concentration of lead in folk remedies and cosmetics used by immigrants from Central and South America, India and Southern Asia. These have many names including sanna and koli. Be sure to ask!
Case History - Part 1
His mother brings Michael W. a 6-year-old African American boy, to your office. Mrs. W. is concerned about Michael's recent performance in school. Marjie reveals that over the past year, Michael's school performance has steadily declined. She is very upset and concerned because Michael had been a straight A student until this point. Michael appears to be a healthy young boy however, he seems distracted and somewhat hyper kinetic.
There is no family history of learning disabilities or mental retardation. Michael's parents have been divorced since he was 2. He primarily lives with his mother in the suburbs but spends his summer vacation and some weekends with his father who lives in the Fort Greene section of Brooklyn. Mrs. W. stresses that she is uncomfortable with the care he receives. She thinks that the problems stem from his father's inability to be a proper parent.
Q1. Based on the presentation and history, what factors indicate lead exposure?
A1. Children exposed to lead often have learning disabilities, cognitive problems and problems with motor developmental status. These children have impaired reaction time under varying intervals of delay, increased distractibility, impulsiveness, aggressiveness and hyperactivity, all which can result in poor school performance as is evident in Michael's case. The parental tensions might be coming into play, but lead poisoning must be considered. Michael housing arrangement should be considered. Disadvantaged communities, such as the inner city, have higher levels of lead exposure than in other communities.
We have chosen an African-American child for this case study as there is a predominance of lead poisoning in African American Communities. Neither the social circumstances (good or bad) nor the race/ethnicity of the family, however, should distract the pediatrician from the possibility of lead poisoning. Do the test!
Q2. What are ways in which children and adults are exposed to lead?
A2. Children are often exposed to lead through lead based paint, plaster dust, and debris peeling off walls and ceilings. Adults can also be exposed in an industrial setting in the production of paint, storage batteries, pottery and the manufacture of solder and brass (Hamilton, 1925).
Q3. When should you perform a lead risk assessment?
A3. According to the CDC 1997 guidelines the questions listed should be asked to screen for lead poisoning. This questionnaire is best used during prenatal care and on the first encounter of the pediatrician with the family
TABLE 1: Standard CDC Screening questions
If the parent answers "yes" or "not sure" to any of these questions their child should be screened for lead poisoning.
At this point, you suspect that Michael has been exposed to lead during his visits to his father. You order a lead test to determine the concentration of lead I Michael's blood.
Q4. What laboratory values on the lead test are considered diagnostic for lead poisoning?
A4. CDC guidelines from 1991 consider elevated blood lead levels below 10 ugm/dL as Class I. Class II is from 10 to 19.9ugm/dL. than 9.9 ugm/dL. They suggest that levels 20 to 45 ugm/dL (Class II) warrant medical and environmental intervention. Levels from 45 to 70 are Class IV require confirmation and chelation therapy. The test itself is imprecise with a 14% error, and chelation is potentially harmful. An above 70 ugm/dL would require confirmation though any Class IV or V children showing signs of encephalopathy should receive immediate chelation therapy while awaiting results much as is done with meningitis.
In truth, these recommendations are archaic. Any child with an elevated blood lead level should have their home and other environments (i.e. daycare, school) investigated. Any level of lead in a child is deleterious to his/her health. Others at the residence should also be tested. Treatment of the source of exposure is mandated because without treatment, re-exposure will likely recur.
Moreover, the level of 10ugm/dL is greater than what we now know to be toxic. The present skill at distinguishing social effects from living in environments were lead is available from neurotoxic effects brings the toxic level to 5 ugm/dL.
Q5. What is a "safe" BLL level?
A5. Although the AAP and CDC suggest that, no action should be taken with BLL levels <10, current thinking is that there is no threshold for lead effects an thus no "safe" blood lead level. Simply stated, the safe [BPb] is zero.
The Case continues
No significant abnormalities are noted on Michael's physical exam, however Michael does appear somewhat pale. You inquire about his eating habits and living conditions. Marjie states that she lives in a private home with her mother and Michael, and provides a somewhat balanced diet. However, she complains that when Michael is with his father, he does not eat as well and the living conditions are not up to par. She knows that Jack's apartment is quite old and has numerous problems such as inadequate ventilation, plumbing, rodents and peeling paint.
Michael's blood lead level returns with the value of 27 ugm/dL. His hemoglobin level is 19.7 g/dL with an MCV of 65 and an RDW of 16.
You inform Mrs. W about your concern for the elevated lead level and probable iron deficiency anemia and suggest the possibility that his behavior has been affected by these two conditions. You draw confirmatory tests - ferritin and iron, iron binding capacity, and percent saturation. These come back with a ferritin of 12ng/dL and a IBC of 7%. Both of these confirm iron deficiency. Prior to receiving results you put Michael on 3 mg/kg of iron and suggest diet changes: Two cups of milk a day. Rice, beans, some meat and fruit or juice at a mid day meal without dairy products.
Mrs. W is quite distraught and has many questions. She's heard about the effects that lead has on a child's learning ability. She ask if the lead could also be the of Michael's unhealthy appearance.
Q6. What are the adverse affects of lead on an individual's health?
A6 Residents in attendance: take a stab at answering this question in groups of 2 or 3. How might iron deficiency and lead poisoning interact to affect Michael's health?
a. Lead is an anti-nutrient.
As a divalent cation, the body in ways that parallel the treatment of other minerals that serve as true nutrients treats it. There are three specific concerns.
1. Lead competes for absorption with other divalent cations such as calcium, iron, and zinc. A dietary deficiency of any one of these nutrients will enhance the absorption of lead and increase the likelihood of lead poisoning.
2. Lead impairment of heme synthesis compounds the effect of iron deficiency resulting in more severe anemia and microcytosis than found with either disturbance alone. Anemia associated with lead poisoning is in reality secondary to iron deficiency.
3. Lead poisoning and iron deficiency each contribute independently to learning failure among children. However, when the conditions co-exist children are four times more likely to show behavioral symptoms usually attributed to lead poisoning.
b. Lead also causes learning failure through changes in temperament, distractibility, impulsiveness, aggressiveness and hyperactivity.
In children, as well as in animal models, lead in relatively low doses affects change in temperament (Needleman, 1988). "Temperament, as defined by Rutter (1987), "is best viewed in terms of a relatively small number of simple, nonmotivational, noncognitive, stylistic features of which emotionality, activity and sociability are the best validated." Needleman (1988) notes that studies of lead exposed primates "… stand in close parallel to the reports of [lead exposed] children of impaired reaction time under varying intervals of delay, and teachers' reports of increased distractibility, impulsiveness, aggressiveness and hyperactivity in classroom."
c. Lead impairs intellectual development.
There are sustained decrements in mental development in infants exposed to maternal blood levels [BPb] of 10 ugm/dl or above. Needleman (1988) and Rosen (1992), who have reviewed the breadth of research on lead and learning, draw the inescapable conclusion that even very tow blood lead levels are associated with decreased cognitive and learning abilities as welt as in motor developmental status. The developmental consequence of low lead exposure is shown in the Figure 1. As Sayre & Emhart (1992) point out, these consequences of low lead level exposure reflect "cluster effects of poverty" which are additive to those seen with lead.
Q7. What are the appropriate steps in treating and managing Jack's lead poisoning? How would you have responded differently if his BLL was higher or lower?
A7. The American Academy of Pediatrics (AAP) has established a table of recommended follow up services for various BLL levels. With a BLL of 15micrograms/dL, the physician should order a confirmatory venous blood test, take an the environmental history, and educate the patient on decreasing blood lead exposure and decreasing lead absorption. The AAP suggests that the BLL should be taken again within 2 months.
The following table contains the recommendations from the AAP for levels up to 45ugm/dL. Children with levels putting them at risk for encephalopathy should be hospitalized for protection, evaluation, and possible chelation therapy.
Table 2. Recommended Follow-up Services, According to Diagnostic BLL
(American Academy of Pediatrics, 1998)
Q8. These suggestion simply that lead levels below 10ugm/dL are harmless. Is that true
A8. No:
The results of the study by Lanphear and colleagues as well as others by Mendelsohn in New York show that there is no threshold. We simply lack tools to identify specific damages at lower levels
Q9. Lead poisoned children are almost always from poor families with little education. African American children are most commonly affected. Might the socioeconomic variable affecting school performance be the predominant effect on learning rather than lead.
A9 Quote "neighborhoods to neurons. And Port Pirie.
Q10. Isn't it possible to improve development by removing lead from the body? How efficient is chelation therapy? What other treatments are required?
A10. Long-term follow up studies of children treated for subclinical lead poisoning show repeated failures in school even among those children whose received chelation therapy. (Rosen, 1992).
All children with lead poisoning should have initial treatment for iron deficiency (2-3mg/kg/day for three months) followed by daily supplementation with a standard vitamin and mineral preparation.
Case Study Continues
Mrs. W believes that Michael is exposed to lead when he visits her former husband's apartment. She is concerned that after Michael is treated and visits his father again he would just be re-exposed to lead. She recognizes now that whatever anger she has should not be directed at him. Rather she needs a plan to get the apartment abated.
She tells you that Mr. W's landlord is hesitant to have the work done professionally. Mr. W, would like to move but he cannot afford to do so. The mother is caught!. She is worried because she cannot refuse to let MR W. see Michael, but she's legitimately concerned about Michael's health.
Q11. How can the issue of hazardous lead paint be addressed legally?
A11. In the New York City Childhood Lead Poisoning Prevention Act of 2003, Local Law 1 was passed to prevent lead paint hazards in housing and day care facilities. The law requires landlords to follow certain rules meant to help prevent children from being lead-poisoned.
The law applies to apartments and common building areas that fit the following criteria:
1. Built before 1960 (or built between 1960 and1978 if your landlord knows that the building contains lead paint),
2. With 3 or more apartments, and
3. Where a child under 7 years of age lives.
Local Law 1 says that landlords must:
1. Find out if a child under 7 lives in any apartment in buildings covered by the law.
2. Inspect those apartments for lead paint hazards.
3. Use safe work practices and trained workers for any work that disturbs lead paint in applicable apartments and common areas, including required repairs of peeling paint.
4. Make apartments "lead safe" on turnover (when a tenant moves out and another moves in).
5. Clean up work areas thoroughly.
6. Have "clearance dust wipe tests" performed when work is finished to make sure cleanup is complete.
7. Keep records of all notices, inspections, and repair of lead paint hazards, and other matters related to the law.
(NYC Dept of Health and Mental Hygiene)
The case concludes with a relatively happy ending:
The father's landlord repaired the lead paint hazards and the DOH inspected the apartment. Two months later, Michael returns to your office with both parents to repeat the lead test. You find that the hemoglobin level has risen Your tell the parents that Michael's prognosis is better, and that they should continue to monitor his diet and behavior. You are cautious about prognosis
Q12. And what is that prognosis?
Again, let residents discuss prior to informing
A12. An unfortunate reality is that lead poisoning occurs at a critical juncture in a child's neurodevelopment. The likely possible outcomes of diminished intellectual functioning, learning disability, and attrition deficit are not entirely predictable. As Ballinger points out, there is no fingerprint to lead poisoning. What happens later depends on timing, elevation and duration. The most common consequences are those that affect executive functioning and auditory processing. The most commonly cited consequnces (decreased "IQ") is the least reliable. Simply stated lead poisoning in childhood, with or without concomitant iron deficiency creates a life long disability.
References:
American Academy of Pediatrics. Screening for Elevated Lead Blood Levels. Pediatrics. 1998, June pp. 1072-1078
Centers for Disease Control and Prevention. Health Topic: Lead.
Available at: http://www.cdc.gov/health/lead.htm
Hamilton, A. The prevalence of industrial lead poisoning in the United States. (in) Aub, Fairhill, Minot and Resnikioff. Lead poisoning. Medicine 1925; 4:218-26.
Lead Poisoning (in) Malnourished Children in the United States: Caught in the cycle of Poverty. Karp
Mahaffey KR. Nutritional factors in lead poisoning. Nutrition Reviews 1981; 39:353-60.
Needleman H. The persistent threat of lead; the medical ad sociological issues. Current Problems in Pediatrics. 1998. December, 702-44.
Rosen J. Health effects of lead at low exposure levels: Expert consensus and rationale for lowering the definition of childhood lead poisoning. Am J Dis Child. 1992; 146:1278-81.
Rutter M. Temperament, personality ad personality disorder. Brit J Psychiatry 1987; 150:443-458.
Sayre, JW Ernhart CB. Control of lead exposure in childhood: are we doing it correctly, Am J Dis Child. 1992; 146: 1275-8.
The New York City Department of Health and Mental Hygiene (2004). Preventing Childhood Lead Poisoning.
Available at: http://www.nyc.gov/html/doh/html/lead/brochure-072004.html
Annotated Pre-test Answers
A1. This is True. Lead us a neurotoxic substance. The only question is "how well can we separate the confounding factors affecting lead poisoned children?"
A2. This is False. Lead poisoning affects children at a critical place in neurodevelopment such that consequences are life long in their own right as well as for the effect they have on the sequence of development.
A3. This is False. Rather it is the landlord's responsibility to have a trained worker certified in abatement procedures. Untrained parents or workers are quite likely to make matters worse.
A4. The answer is C. Encephalopathy has been found at this level. Always recheck, as there is a 14% error in measurement and false positive measures are possible, and chelation is by no means innocuous.
