Fatal Pediatric Lead Poisoning --- New Hampshire, 2000
Fatal pediatric lead poisoning is rare in the United States because of multiple public health measures that have reduced blood lead levels (BLLs) in the population. However, the risk for elevated BLLs among children remains high in some neighborhoods and populations, including children living in older housing with deteriorated leaded paint. This report describes the investigation of the first reported death of a child from lead poisoning since 1990 (1). The investigation implicated leaded paint and dust in a home environment as the most likely source of the poisoning. Lead poisoning can be prevented by correcting lead hazards, especially in older housing, and by screening children at risk according to established guidelines (2).
On March 29, 2000, a 2-year-old girl was seen at a community hospital emergency department with a low-grade fever and vomiting of approximately 1 day's duration. The child had been well since arriving in New Hampshire from Egypt with her Sudanese refugee family 3 weeks earlier. Laboratory findings included a microcytic anemia (hemoglobin: 7.6 g/dL; lower limit of normal: 11.5 g/dL) with occasional basophilic stippling of red blood cells. A throat swab streptococcal antigen screening test was positive. She was discharged from the emergency department with prescriptions for an antibiotic and antiemetic to treat presumed strep throat. However, her vomiting worsened, and she was admitted to the same hospital on April 17, and then transferred to a tertiary-care hospital the next day. On April 19, approximately 5 hours after the transfer, she became unresponsive, apneic, and hypotensive. She was intubated and placed on a ventilator. Computerized tomography of the head showed diffuse cerebral edema and dilated ventricles. Later that day, the results of a blood test drawn on April 18 showed a BLL of 391 µg/dL and an erythrocyte protoporphyrin level of 541 µg/dL. Chelation therapy was initiated with intramuscular British antilewisite and intravenous calcium ethylenediaminetetraacetic acid. Despite a decrease in her BLL to 72 µg/dL and treatment for increased intracranial pressure, including surgical ventricular drainage, she remained comatose without spontaneous respirations, brain electrical activity, and intracranial blood flow. She was pronounced brain dead on April 21.
An autopsy found diffuse cerebral edema. A hair sample lead concentration was 31 µg/g in the distal centimeter and 67 µg/g in the proximal centimeter, indicating a large increase in lead exposure during the preceding month. Radiographs of the left knee were equivocal for growth arrest lines that can occur in chronic lead poisoning (3). A bone marrow sample showed no stainable iron, indicating iron deficiency.
On April 19, the Manchester Health Department and New Hampshire Department of Health and Human Services (NHDHHS) initiated an investigation, including interviews and blood lead tests of the patient's family and an inspection of her residence. In addition, to assess a possible contribution of lead exposure from the child's previous residence in Egypt, the Field Epidemiology Training Program of the Egyptian Ministry of Health obtained soil and dust samples from that location.
After living in Egypt for approximately 18 months, on March 9, 2000, the family had moved to Manchester into an apartment constructed before 1920. A wall in a sibling's bedroom had multiple holes from which the patient had been seen removing and ingesting plaster. Two of seven samples of plaster with the adhering surface paint contained lead at levels of 5% and 12%. Peeling paint (35% lead) was present on the balusters and floor (3% lead) of a porch outside the apartment entrance where the patient sometimes had played. She also had played near and looked out of a living room window that occasionally was opened during meal preparation. A wipe sample of dust from the window well showed 6732 µg lead/ft2, well above the hazardous level of 800 µg/ft2 (4). NHDHHS ordered the apartment owner to correct the lead hazards identified during the inspection. The patient's family relocated to another dwelling.
BLLs in the mother and three siblings (ages 5, 11, and 15 years) ranged from 4--12 µg/dL. The family did not use or possess nontraditional remedies, food supplements, cosmetics, or ceramic eating or drinking containers acquired abroad. No one in the household was employed or had lead-related hobbies. Measurements of stable lead isotopes (5) in selected environmental samples and the patient's blood showed that the isotopic lead composition of the porch paint and window well dust in the her Manchester apartment matched the composition of lead in her blood more closely than did the isotopic composition of other samples, including those from her previous residence in Egypt.
Reported by: RM Caron, PhD, R DiPentima, MPH, C Alvarado, P Alexakos, Manchester Health Dept, Manchester; J Filiano, MD, Dartmouth Hitchcock Medical Center, West Lebanon; T Gilson, MD, Office of the Chief Medical Examiner; J Greenblatt, MD, G Robinson, N Twitchell, L Speikers, New Hampshire Dept of Health and Human Svcs. MA Abdel-Nasser, MD, HA El-Henawy, MD, Field Epidemiology Training Program, Ministry of Health, Egypt. M Markowitz, MD, Montefiore Medical Center, New York. P Ashley, US Dept of Housing and Urban Development. Div of Environmental Hazards and Health Effects, Div of Laboratory Sciences, National Center for Environmental Health, CDC.
Lead encephalopathy is a life-threatening complication of lead poisoning that can occur in young children who have very high BLLs (>70--100 µg/dL). Nonspecific symptoms (e.g., lethargy, sporadic vomiting, and constipation) can occur at BLLs >50--70 µg/dL and may precede the abrupt onset of frank encephalopathy characterized by persistent vomiting, ataxia, altered consciousness, coma, and seizures. In this report, the child's anemia with basophilic stippling also suggested lead poisoning. However, symptoms or signs cannot be used to reliably diagnose or exclude lead poisoning; a BLL must be measured whenever lead poisoning is suspected. In young children, BLLs >70 µg/dL or elevated BLLs with symptoms suggesting encephalopathy require prompt inpatient treatment with chelating agents to rapidly reduce BLLs. Providing appropriate intensive care for children with encephalopathy can prevent death, although severe permanent brain damage can occur despite treatment (3).
During the 1950s and 1960s, acute, often fatal, lead encephalopathy was a common cause of pediatric admissions to urban hospitals (6). The subsequent decline in fatal lead poisoning cases is attributable to reduced lead exposure from multiple sources, institution of lead screening programs, and improved treatment of lead poisoning (6). Despite the reduction in severe lead poisoning, in some U.S. counties, >20% of young children tested have BLLs >10 µg/dL (7), high enough to adversely affect learning and development (3).
The likely sources of lead poisoning for the child in this report---deteriorated leaded paint and elevated levels of lead-contaminated house dust---are found in an estimated 24 million U.S. dwellings, 4.4 million of which are home to one or more children aged <6 years (U.S. Department of Housing and Urban Development, unpublished data, 2001). Lead hazards are especially common in homes built before 1960 (58%). Although the patient's pica and iron deficiency probably contributed to the severity of her lead poisoning, by increasing ingestion and absorption of lead (3), all children living in homes with lead hazards are at increased risk for developing elevated BLLs (8).
Children who are refugees, adoptees, or recent immigrants may be at increased risk for elevated BLLs, possibly related to lead exposure in their country of origin or to continued use of certain lead-containing traditional remedies or cosmetics. However, such children also are at risk for exposure to leaded paint hazards in older U.S. housing. In addition to ensuring that such children are screened after arrival in the United States, lead poisoning prevention programs and health-care providers should ensure that families receive timely education about lead hazards. Federal regulations require that property sellers and landlords provide families with information about lead poisoning and about any known lead hazards in a dwelling before its sale or lease.* Agencies providing health and social services to refugees and immigrants should become familiar with these regulations and ensure that appropriate information is provided to families in a language they can understand.
- CDC. Fatal pediatric poisoning from leaded paint---Wisconsin, 1990. MMWR 1990;40:193--5.
- CDC. Screening young children for lead poisoning: guidance for state and local public health officials. Atlanta, Georgia: US Department of Health and Human Services, CDC, 1997.
- CDC. Preventing lead poisoning in young children: a statement by the Centers for Disease Control, October 1991. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, CDC, 1991.
- US Department of Housing and Urban Development (HUD). Guidelines for the evaluation and control of lead-based paint hazards in housing. Washington, DC: US Department of Housing and Urban Development, 1995. Available at http://www.hud.gov/lea/learules.html#download. Accessed February 22, 2001.
- Chaudhary-Webb M, Paschal DC, Elliott WC, et al. ICP-MS determination of lead isotope ratios in whole blood, pottery, and leaded gasoline: lead sources in Mexico City. Atomic Spectroscopy 1998;19:156--63.
- Lin-Fu JS. Modern history of lead poisoning: a century of discovery and rediscovery. In: Needleman HL, ed. Human lead exposure. Boca Raton, Florida: CRC Press, 1992.
- CDC. Blood lead levels in young children---United States and selected states, 1996--1999. MMWR 2000;49:1133--7.
- Lanphear BP, Matte TD, Rogers J, et al. The contribution of lead-contaminated house dust and residential soil to children's blood lead levels: a pooled analysis of 12 epidemiologic studies. Environ Res 1998;79:51--68.
*24 CFR Part 35, 40 CFR Part 745.
All MMWR HTML versions of articles are electronic conversions from typeset documents.
This conversion might result in character translation or format errors in the HTML version.
Users are referred to the electronic PDF version (http://www.cdc.gov/mmwr)
and/or the original MMWR paper copy for printable versions of 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 firstname.lastname@example.org.