Persons using assistive technology might not be able to fully access information in this file. For assistance, please send e-mail to: firstname.lastname@example.org. Type 508 Accommodation and the title of the report in the subject line of e-mail.
Epidemiologic Notes and Reports Fatal Pediatric Poisoning from Leaded Paint -- Wisconsin, 1990
Although fatal lead poisoning among children occurs rarely in the United States, it represents a medical and public health emergency. This report summarizes the investigation of a child who died from poisoning associated with ingestion of leadbased paint.
On September 12, 1990, a 28-month-old Wisconsin boy was admitted to a hospital with a 4-day history of lethargy and reduced appetite. Although the child had no known past medical problems, his parents reported that he had eaten flaking paint. On initial neurologic examination, the child had extreme lethargy with facial palsy and gasping respirations, consistent with lead encephalopathy; laboratory results revealed severe lead toxicity and hematologic abnormalities (blood lead level (BLL) 144 ug divided by L; erythrocyte protoporphyrin level 593 ug divided by L; hemoglobin 8.1; and basophilic stippling). Despite chelation therapy with British antilewisite and calcium disodium edetate (CaNa 2-EDTA), the child developed seizures, became comatose, and died 26 hours after admission. An autopsy showed massive cerebral edema with uncal herniation. The intestines contained multiple roundworms (Ascaris lumbricoides) and flake-like material consistent with paint chips. Radiographs revealed prominent epiphyseal lines in the lower extremities, consistent with chronic lead exposure.
On September 20, staff from the Wisconsin Division of Health and the Waukesha County Health Department inspected the child's residence. The child and his parents had lived for at least 4 months on the second floor of a two-story, nonresidential structure built in 1923. The interior paint was badly deteriorated with paint chips visibly flaking from the walls and accumulating on floors, windowsills, and stairs. Eleven paint chip samples from the apartment ranged from 0.2% to 33.1% lead by weight (average: 9.1%); the U.S. Consumer Product Safety Commission (CPSC) permits a maximum of 0.06% lead in new residential paint.* House dust from the child's bedroom floor contained 3900 ug lead/ft2, and dust from a windowsill above the child's bed contained 31,128 ug lead/ft2. These levels are more than 10 times higher than those proposed in recent guidelines issued by the U.S. Department of Housing and Urban Development (1), which recommend the maximum dust lead levels permissible before reoccupancy of a unit following lead paint abatement.
After the child's death, the parents moved and were unavailable for follow-up. The landlord has blocked access to the second floor and plans to eliminate the lead paint hazards in the building. Reported by: J Schirmer, MS, HA Anderson, MD, State Environmental Epidemiologist, Div of Health, Wisconsin Dept of Health and Social Svcs; LA Saryan, PhD, Industrial Toxicology Laboratory, West Allis Memorial Hospital, West Allis, Wisconsin. Lead Poisoning Prevention Br, Center for Environmental Health and Injury Control, CDC.
Editorial Note: Lead encephalopathy usually is associated with a BLL greater than 100 ug divided by L, although it has been reported at BLLs as low as 70 ug divided by L (2). As in this report, children with acute lead encephalopathy often have a recent history of prodromal symptoms, including anorexia, apathy, decreased play activity, hyperirritability, aggressiveness, poor coordination, and sporadic vomiting. Because lead encephalopathy in a child can rapidly progress to death, either a BLL greater than or equal to 70 ug divided by L in a child or the onset of encephalopathy constitutes an acute medical emergency.
At least four factors may account for the dramatic decline in the incidence of acute lead encephalopathy and childhood deaths from lead poisoning since the 1960s (3), including 1) increased screening of children at risk, 2) recognition of toxicity before the onset of life-threatening symptoms, 3) improvements in the treatment for lead poisoning, and 4) reduction of lead exposure from certain environmental sources. Although childhood deaths from poisoning associated with exposure to lead-based paint are now rare in the United States (4) (the most recently reported lead-based paint-associated death occurred in the mid-1970s (5)), subclinical toxicity is a widespread and persistent public health problem (6). BLLs as low as 10 ug divided by L, once considered safe, are now known to adversely affect cognitive development and behavior in children (7), with potentially long-term sequelae (8). In 1984, an estimated 3-4 million U.S. children had BLLs greater than or equal to 15 ug divided by L (6).
The primary source of high-dose lead exposure among children in U.S. urban areas is lead-based paint (6). Although CPSC banned lead-based paint for residential use in 1978, an estimated 12 million children less than 7 years of age reside in homes containing previously applied lead-based paint (6). Interior paints used before 1940 contained as much as 50% lead (9). Although children can ingest lead directly by eating paint chips, ingestion of lead-contaminated house dust and soil during normal mouthing and exploratory behaviors contributes substantially to elevating BLLs (10). The child reported in Wisconsin appeared to have been ingesting paint chips and was exposed to highly contaminated house dust.
All cases of lead poisoning are preventable. A national health objective for the year 2000 is to reduce the prevalence of children aged 6 months through 5 years with BLLs greater than 15 ug divided by L to less than 500,000 and the prevalence of those with BLLs greater than 25 ug divided by L to zero (11). Recently, several federal agencies responsible for housing, health, and the environment have focused attention on this problem and have set goals to abate lead-based paint in privately owned housing (12), reduce the number of children with elevated BLLs (13), and promote national efforts to eliminate childhood lead poisoning (14).
guidelines for hazard identification and abatement in public and Indian housing. Washington, DC: US Department of Housing and Urban Development, Office of Public and Indian Housing, 1990.
2. Piomelli S, Rosen JF, Chisolm JJ, Graef JW. Management of childhood lead poisoning. J Pediatr 1984;105:523-32.
3. Lin-Fu JS. The evolution of childhood lead poisoning as a public health problem. In: Chisolm JJ, O'Hara DM, eds. Lead absorption in children: management, clinical and environmental aspects. Baltimore: Urban and Schwarzenberg, Inc, 1982:1-10.
4. NCHS. Vital statistics mortality data, multiple cause-of-death detail (machine-readable public-use data tape). Hyattsville, Maryland: US Department of Health and Human Services, Public Health Service, CDC, 1979-1987.
5. Klein R. Lead poisoning. In: Barness LA, ed. Advances in pediatrics. Vol 24. Chicago: Year Book Medical Publishers, 1977:103-32.
6. 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 Department of Health and Human Services, Agency for Toxic Substances and Disease Registry, 1988.
7. 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 poisoning. Environ Res 1989;50:11-36.
8. Needleman HL, Schell A, Bellinger D, Leviton A, Allred EN. The long-term effects of exposure to low doses of lead in childhood, an 11-year follow-up report. N Engl J Med 1990;322:83-8.
9. National Academy of Sciences. Report of the Ad Hoc Committee to Evaluate the Hazard of Lead in Paint. Washington, DC: US Consumer Product Safety Commission, 1973:3. 10. Charney E, Sayre J, Coulter M. Increased lead absorption in inner city children: where does the lead come from. Pediatrics 1980;65:226-31. 11. Public Health Service. Healthy people 2000: national health promotion and disease prevention objectives. Washington, DC: US Department of Health and Human Services, Public Health Service, 1990; DHHS publication no. (PHS)90-50212. 12. Office of Policy Development and Research. Comprehensive and workable plan for the abatement of lead-based paint in privately owned housing: a report to Congress. Washington, DC: US Department of Housing and Urban Development, Office of Policy Development and Research, 1990. 13. Environmental Protection Agency. Strategy for reducing lead exposures. Washington, DC: US Environmental Protection Agency, 1991. 14. CDC. Strategic plan for the elimination of childhood lead poisoning. Atlanta: US Department of Health and Human Services, Public Health Service, 1991.
Disclaimer All MMWR HTML documents published before January 1993 are electronic conversions from ASCII text into HTML. This conversion may have resulted in character translation or format errors in the HTML version. Users should not rely on this HTML document, but are referred to the original MMWR paper copy for the official text, figures, and tables. An original paper copy of this issue can be obtained from the Superintendent of Documents, U.S. Government Printing Office (GPO), Washington, DC 20402-9371; telephone: (202) 512-1800. Contact GPO for current prices.**Questions or messages regarding errors in formatting should be addressed to email@example.com.
Page converted: 08/05/98
This page last reviewed 5/2/01