Preventing Lead Poisoning in Young Children -- United States

CDC has issued a new statement on preventing lead poisoning in young children (1). This statement replaces the 1978 statement (2), which defined levels for elevated blood lead, undue lead absorption, lead toxicity, and lead poisoning. The 1985 statement is intended to serve as a guideline for lead-poisoning prevention programs in the United States.

Since 1978, investigators have reported adverse effects from low-level lead exposure on children's behavior and intelligence (3), hemoglobin formation in red blood cells (4), and metabolism of vitamin D (5). These studies demonstrate that little or no margin of safety is associated with a level of 30 micrograms of lead per deciliter (ug/dl) of whole blood--the lowest level defined as elevated in CDC's 1978 statement.

To be successful, a screening program designed to prevent childhood lead poisoning requires, not only an acceptable and cost-effective screening procedure, but also medical follow-up and means of preventing the child from future exposure to lead (6). The erythrocyte protoporphyrin (EP) test is recommended as the screening test for lead toxicity because it can be easily performed on a drop of blood obtained from a finger prick and placed in a portable fluorometer. Since EP levels increase in both lead poisoning and iron deficiency, follow-up testing for elevated blood lead and/or iron deficiency must be done.

Some major changes in the 1985 statement compared with the 1978 statement are:

1. An elevated blood lead level, which reflects excessive absorption of lead, is defined as a concentration of lead in whole blood of 25 ug/dl or greater (formerly 30 ug/dl or greater).

2. Lead toxicity is defined as an elevated blood lead level with an EP level in whole blood of 35 ug/dl or greater (formerly 50 ug/dl or greater).

3. Lead is most harmful to children between the ages of 9 months and 6 years. Ideally, all children should be screened. As more children are screened for iron deficiency by EP testing, simultaneous lead screening of these same groups becomes feasible.

4. For EP levels greater than 35 ug/dl, EP values obtained with hematofluorometers are generally lower than EP values obtained by the extraction method. Therefore, separate cut-off levels are used for classifying the urgency of medical follow-up.

5. Greater reliance is placed on the calcium disodium EDTA mobilization ("Provocative Chelation") test in determining whether a full course of chelation therapy is indicated for children with blood lead levels in the 25-55 ug/dl range. The revised lead statement, Preventing Lead Poisoning In Young Children: A Statement by the Centers for Disease Control: January 1985, will be available on request after March 1, 1985, from: Publication Activities, Center for Environmental Health, Centers for Disease Control, Atlanta, Georgia 30333; (404) 452-4102. Reported by Special Studies Br, Chronic Diseases Div, Center for Environmental Health, CDC.

   Editorial Note

Editorial Note: The second National Health and Nutrition Examination Survey (NHANES II, 1976-1980) found that children from all geographic and socioeconomic groups are at risk of lead poisoning (7). An estimated 3.9% (or nearly one of 25) of the children in the United States under 5 years of age had blood lead levels of 30 ug/dl or greater--levels possibly causing adverse physiologic and neurobehavioral effects. Between 1976 and 1980, the overall mean blood lead levels dropped from 14.6 ug/dl to 9.2 ug/dl, and this corresponded with a decline in the sales of leaded gasoline during this period (8).

Lead-based paint continues to be the major source of high-dose lead exposure and asymptomatic lead poisoning for children in the United States. Since 1977, paint produced for household use must, by regulation, contain no more than 0.06% (600 parts per million ]ppm^) lead by dry weight, but some paints manufactured in the 1940s for indoor use contained more than 50% (500,000 ppm) lead. An estimated 27,000,000 households in this country remain contaminated by lead paint (9).

Typically, symptomatic lead poisoning occurs among children under 6 years old living in deteriorated, pre-World War II housing. Repeated ingestion of nonfood substances has been shown to be associated with lead poisoning in young children (10), but it is not a prerequisite for lead poisoning (11), since children's normal mouthing behavior alone is sufficient to cause those living in contaminated homes to have high lead exposure. Lead poisoning has been reported in children whose parents moved to a city as "urban homesteaders"; the children were exposed to chips, dust, or fumes from lead-based paint when the old houses were remodeled or renovated (10).

Other potential sources of lead exposure include the use of imported lead-glazed pottery for cooking (12) or storing food and hobbies and activities involving lead, such as working with stained glass or casting lead objects.

The highest priority for screening should be given to 12- to 36-month-old children who live in or frequently visit older, dilapidated housing, who live near lead smelters or other industrial sources of lead, or whose parents work with materials containing lead.

Screening all children for lead toxicity--including those not suspected of having been exposed to lead--is feasible, since the EP test can also be used as the screening for iron deficiency. Recently, in a nutritional assistance program, the EP test was used to screen children for iron deficiency (13), and some Hmong refugee children were found to have lead toxicity. The source was traced to a Hmong folk remedy used for treating infants and children with fevers.

References

1. CDC. Preventing lead poisoning in young children: a statement by the Centers for Disease Control: January 1985. Atlanta, Georgia: Department of Health and Human Services, 1985.

2. CDC. Preventing lead poisoning in young children: a statement by the Center for Disease Control: April 1978. Atlanta, Georgia: Department of Health, Education, and Welfare, 1978.

3. Needleman HL, Gunnoe C, Leviton A, et al. Deficits in psychologic and classroom performance of children with elevated dentine lead levels. N Engl J Med 1979;300:689-95.

4. Piomelli S, Seaman C, Zullow D, Curran A, Davidow B. Threshold for lead damage to heme synthesis in urban children. Proc Natl Acad Sci USA 1982;79:3335-9.

5. Rosen JF, Chesney RW, Hamstra A, DeLuca HF, Mahaffey KR. Reduction in 1,25-dihydroxyvitamin D in children with increased lead absorption. N Engl J Med 1980;302:1128-31.

6. Piomelli S, Rosen JF, Chisolm JJ Jr, Graef JW. Management of childhood lead poisoning. J Pediatr 1984;105:523-32.

7. 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. N Engl J Med 1982;307:573-9.

8. Annest JL, Pirkle JL, Makuc D, Neese JW, Bayse DD, Kovar MG. Chronological trend in blood lead levels between 1976 and 1980. N Engl J Med 1983;308:1373-7.

9. Lin-Fu JS. Children and lead: new findings and concerns ]Editorial^. N Engl J Med 1982;307:615-7.

10. Chisolm JJ Jr, O'Hara DM, eds. Lead absorption in children: management, clinical, and environmental aspects. Baltimore, Maryland: Urban & Schwarzenberg, 1982.

11. Sayre JW, Charney E, Vostal J, Pless IB. House and hand dust as a potential source of childhood lead exposure. Am J Dis Child 1974;127:167-70.

12. Bird TD, Wallace DM, Labbe RF. The porthyria, plumbism, pottery puzzle. JAMA 1982;247:813-4.

13. CDC. Folk remedy-associated lead poisoning in Hmong children--Minnesota. MMWR 1983;32:555-6.

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