Published online October 1, 2004
PEDIATRICS Vol. 114 No. 4 October 2004, pp. 1096-1099 (doi:10.1542/peds.2004-0361)
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EXPERIENCE AND REASON

Lead Poisoning From a Toy Necklace

Jessica L. VanArsdale, MD, MPH*, Richard D. Leiker, MS{ddagger}, Mel Kohn, MD, MPH§, T. Allen Merritt, MD, MHA||,¶ and B. Zane Horowitz, MD#

* Departments of Family Medicine and Public Health and Preventive Medicine
# Oregon Poison Center, Oregon Health and Science University, Portland, Oregon
{ddagger} Oregon Childhood Lead Poisoning Prevention Program
§ Disease Prevention and Epidemiology, Oregon Department of Human Services, Oregon Health Services, Portland, Oregon
|| St Charles Medical Center and Central Oregon Pediatric Associates, Bend, Oregon
Oregon Commission for Children and Families, Portland, Oregon


   ABSTRACT
TOP
 ABSTRACT
CASE REPORT
 DISCUSSION
 CONCLUSIONS
 REFERENCES
 
A 4-year-old, previously healthy boy experienced intermittent abdominal pain for several weeks. He was diagnosed with probable gastroenteritis, but his symptoms worsened. Laboratory tests revealed normocytic anemia, and an abdominal radiograph showed a metallic foreign body in the stomach, without evidence of obstruction. Endoscopy resulted in the retrieval of a quarter and a medallion pendant from the stomach. A venous blood lead level measurement was extremely elevated, at 123 µg/dL (level of concern: ≥10 µg/dL). The medallion was tested by the state environmental quality laboratory and was found to contain 38.8% lead (388 000 mg/kg), 3.6% antimony, and 0.5% tin. Similar medallions purchased from toy vending machines were analyzed and were found to contain similarly high levels of lead. State health officials notified the US Consumer Product Safety Commission, which resulted in a national voluntary recall of >1.4 million metal toy necklaces.

Key Words: lead • lead poisoning • lead foreign bodies

Abbreviations: LFB, lead foreign body • BLL, blood lead level • EDTA, calcium disodium versenate • ZPP, zinc protoporphyrin • RBC, red blood cell

Pediatric lead poisoning remains an important preventable public health problem. Children can be exposed to lead through a variety of sources. Although ingestion of dust from lead-based paint remains the most significant source of lead exposure among children, lead can be present in unsuspected objects that, when ingested, can result in rapid lead poisoning. The diagnosis of lead poisoning resulting from ingestion of lead foreign bodies (LFBs) is often delayed when lead poisoning is not included in the differential diagnosis for the presenting symptoms. Appropriate management and follow-up procedures have changed during the years, and it is important for pediatric health care providers to be aware of these changes. This case report describes a child with lead poisoning after ingestion of a medallion necklace purchased from a toy vending machine. We discuss management and follow-up procedures for children with foreign-body ingestion.


   CASE REPORT
TOP
 ABSTRACT
 CASE REPORT
DISCUSSION
 CONCLUSIONS
 REFERENCES
 
A 4-year-old, previously healthy boy was brought to his physician after several days of abdominal cramping, vomiting, and diarrhea without fever. Probable viral gastroenteritis was diagnosed, and the patient's symptoms resolved during the following week. The patient remained asymptomatic for 1 to 2 weeks until he experienced another bout of vomiting and abdominal pain. He returned to his physician, and an abdominal ultrasound scan revealed a normal appendix with mesenteric adenitis. The results of a complete blood count and metabolic panel were normal except for normocytic anemia (hemoglobin: 9.9 g/dL; hematocrit: 28.4%; mean corpuscular volume: 83 fL) and mild elevation of liver enzyme levels (aspartate aminotransferase: 76 U/L; alanine aminotransferase: 120 U/L). Probable viral syndrome causing mesenteric adenitis and anemia of undetermined cause were diagnosed. Two days later, the patient was brought to the local emergency department with symptoms of increasing abdominal pain, protracted vomiting, decreased urine output during the previous 48 hours, no bowel movements for 5 days, and a 4- to 5-lb weight loss during the previous week. The patient exhibited increased irritability and was unable to eat or sleep because of the abdominal pain. His physical examination was notable for a somewhat emaciated appearance, diminished bowel sounds, and abdominal tenderness with deep palpation. An abdominal radiograph showed a metallic foreign body in the stomach, without evidence of obstruction. A repeat blood count and metabolic panel showed persistent normocytic anemia (hemoglobin: 9.5 g/dL; hematocrit: 27.5%; mean corpuscular volume: 82 fL), with some improvement in liver enzyme levels (aspartate aminotransferase: 50 U/L; alanine aminotransferase: 80 U/L). The patient was admitted to the hospital for intravenous hydration and surgical consultation regarding the gastric metallic foreign body. The initial surgical consultation revealed benign abdominal findings, and it was suggested that the object would most likely pass on its own, without necessitating surgical intervention. The following day, an abdominal computed tomography scan showed that the metallic object was more superiorly located, in comparison with findings from the plain film from the previous day. Endoscopy was performed, which resulted in retrieval of a quarter and a medallion pendant from the stomach. The patient was discharged from the hospital but returned to his physician 3 days later, with edema of the left cheek and gingiva. He was thought to have either a dental abscess or excessive biting of the cheek. A pediatric dentist was consulted, and dental radiographs excluded the possibility of a dental abscess. There was concern that the cheek bite could have been attributable to a seizure, which prompted assessment of the blood lead level (BLL). The BLL was extremely elevated at 123 µg/dL (level of concern: ≥10 µg/dL). The child was admitted to the pediatric intensive care unit for intravenous chelation therapy. A neurology consultation revealed no evidence of encephalopathy, and results of a sleep electroencephalogram were normal. The patient was treated with dimercaprol for 48 hours and with calcium disodium versenate (EDTA) for 4 days, and the BLL decreased to 57 µg/dL. The patient was switched to orally administered succimer but required a repeat course of EDTA when the BLL rebounded to 69 µg/dL. After three 19-day courses of succimer, the BLL remained at <40 µg/dL (Fig 1). Iron studies showed no evidence of iron deficiency anemia. Zinc protoporphyrin (ZPP) levels peaked at 556 µmol/mol (normal: 25-65 µmol/mol). Peripheral blood smears showed basophilic stippling.


Figure 1
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  		Fig 1. Venous BLLs for a 4-year-old child in Oregon, 2003.

 
Environmental investigation of the child's home by the public health department did not reveal any additional sources of lead exposure; the home was built in 1996. The child's 6-year-old sibling had a BLL of <5 µg/dL. The child underwent neurodevelopmental, cognitive, and speech therapy evaluations, which showed appropriate development.

The medallion retrieved from the child's stomach reportedly had been purchased from a toy vending machine in Deschutes County, Oregon. It was estimated that the patient ingested the medallion ~3 weeks before it was retrieved. The medallion was tested by the state environmental quality laboratory and was found to contain 38.8% lead (388 000 mg/kg), 3.6% antimony, and 0.5% tin. Two similar medallions purchased from toy vending machines in other parts of Oregon were analyzed and were found to contain similarly high levels of lead (44% and 37%). These medallions are round, ~ 7/8 inch in diameter, and gray in color, with a symbol on 1 side (Figs 2 and 3). State health officials notified the US Consumer Product Safety Commission and an investigation was initiated, which resulted in a national voluntary recall of >1.4 million metal toy necklaces. A distributor of these medallions reported that they are manufactured in India and distributed throughout the United States.


Figure 2
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  		Fig 2. Medallion retrieved from the child's stomach. Analysis by the state environmental quality laboratory found the medallion to contain 38.8% lead (388 000 mg/kg), 3.6% antimony, and 0.5% tin.

 

Figure 3
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  		Fig 3. Medallions purchased from toy vending machines in Oregon. Analysis by the state environmental quality laboratory found the medallions to contain 37% to 44% lead.

 

   DISCUSSION
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 ABSTRACT
 CASE REPORT
 DISCUSSION
CONCLUSIONS
 REFERENCES
 
Foreign-body ingestion is a common occurrence in the pediatric population. In 2002, the American Association of Poison Control Centers received >80 000 calls regarding ingestion of foreign bodies, toys, and miscellaneous objects by children <6 years of age.1 The findings in this case underscore the fact that lead poisoning can occur as a result of ingestion of seemingly innocuous objects. There have been reports of lead poisoning resulting from ingestion of curtain weights, fishing sinkers, lead shot/pellets, key chain emblems, toy sailboat ballasts, and clothing accessories.2–11

In the literature, there are 2 case reports of lead poisoning that was not suspected on the basis of the child's clinical presentation and resulted in death after ingestion of LFBs. Hugelmeyer et al4 described a 23-month-old girl who died as a result of lead encephalopathy after ingestion of a lead curtain weight, which resulted in a BLL of 238 µg/dL. Although the child presented with classic symptoms of lead poisoning, including irritability, lethargy, vomiting, abdominal pain, and seizures, as well as anemia and abdominal radiographic results showing a metallic foreign body in the right upper quadrant, the possibility of lead poisoning was not entertained until after the child's death. The lead curtain weight was thought to have been ingested ~4 weeks before death.4 A similar case was reported by Forsby et al,5 who described a 2-year-old girl with a 10-day history of vomiting who died within 24 hours after hospital admission. The postmortem examination revealed evidence of encephalopathy and a lead drapery weight in the patient's stomach.5 Delayed diagnosis and treatment were common among the published case reports, because lead poisoning was not included in the differential diagnosis for the presenting symptoms.

Acute lead poisoning can cause symptoms such as irritability, lethargy, abdominal pain, constipation, and vomiting, all of which are nonspecific symptoms usually attributed to gastroenteritis. If the condition is not recognized in the early phase of gastrointestinal symptoms, then lead encephalopathy may ensue, causing ataxia, hyperirritability, stupor, and seizures. This may occur at BLLs of >70 to 80 µg/dL.12 Acute levels of >100 µg/dL have been associated with coma and death resulting from cerebral edema. As the reported case illustrates, not all children with very high BLLs become encephalopathic; this is because lead follows a multicompartmental model of tissue entry. Acutely absorbed lead is distributed first to the blood, where 98% of the lead becomes bound in the red blood cells (RBCs), leaving only a small fraction available for distribution to soft tissues such as the brain and kidneys. Lead readily and rapidly crosses the blood-brain barrier, however, and is quickly transported into neurons by efficient metabolic pumps. It is likely that physiologically significant concentrations of lead are deposited in the brain and other soft-tissue compartments even with acute elevations in BLLs. With long-term exposure, lead enters the deeper compartment of bone, which has a prolonged excretion half-life.12 If a BLL measured early after ingestion of an LFB is significantly elevated but the child is asymptomatic, then lead resides mostly in the blood compartment, where it can be easily chelated and removed before it becomes a chronic source of exposure for the patient. Elevated ZPP levels reflect lead bound to intercellular globins in RBCs; levels increase slowly as RBCs are produced in marrow that has elevated levels of lead stored in it. The reported child's elevated ZPP levels and frequent rebounds of BLLs after chelation suggest that he had elevated soft-tissue stores, which may reflect either prior unrecognized ingestions of lead or some lead deposition in brain and other soft tissues as a result of delayed recognition of the LFB ingestion.

Recent studies showed that lead can cause intellectual impairment even among children with BLLs of ≤10 µg/dL.13 The long-term effects of acute lead poisoning, such as described in this report, are unclear, because long-term follow-up monitoring after acute lead intoxication has not been performed systematically. Current guidelines call for any child who has ever exhibited an elevated BLL (>10 µg/dL) to receive long-term neurodevelopmental and behavioral surveillance, because there may be a lag of several years before problems become evident.14 The frontal lobes are particularly vulnerable to the effects of lead poisoning, and lead neurotoxicity can result in disruption of executive functions, attention, social-behavior conduct, and impulse control, which may not be fully appreciated until late childhood or adolescence.15 Tests for executive functioning are not available for children as young as the child described in this case report; therefore, close follow-up monitoring is important. Any child who has ever exhibited an elevated BLL should have this listed on their medical problem list, even after the BLL returns to normal.

Recommended management of LFB ingestion has changed over the years, and there may be misconceptions about appropriate management. In 1989, Durback et al16 suggested that solid lead objects could be retained safely in the bowels for up to 2 weeks without causing lead toxicity. The prevailing thought was that metallic lead and lead alloys were poorly absorbed after ingestion. In a more recent report, Fergusson et al7 proposed that management of LFBs depends on the location. Lead objects located in the stomach pose a higher risk of lead poisoning, compared with lead objects located more distally in the gastrointestinal tract. The acidic environment in the stomach aids dissolution of the lead object, allowing the dissolved lead to pass into the duodenum, where it is absorbed into the bloodstream. For LFBs located in the stomach, those authors suggested treatment with a proton pump inhibitor, to decrease the rate of dissolution, and a prokinetic agent, to encourage passage of the LFB. Repeat radiographs should be obtained 48 hours after ingestion; if the LFB remains in the stomach, then it should be removed endoscopically. Those authors also proposed that other indications for prompt removal include a BLL of >55 µg/dL or symptoms of lead poisoning. For LFBs located in the small intestine, they suggested that the child be given a cathartic agent and observed for passage of the object with abdominal radiographs and BLL measurements every 4 days.7

It may be advisable, however, to monitor BLLs more frequently in the first few days after ingestion, because levels can increase rapidly after ingestion. Published experience suggests that ingestion of LFBs often results in BLLs of >55 µg/dL, for which retrieval is indicated. A case report by Treble and Thompson10 suggests that BLLs can increase rapidly even when the LFB is located in the large intestine. Those authors reported a BLL of 56 µg/dL for a 2.5-year-old child only 1.5 hours after ingestion of pellets from an air rifle. An abdominal radiograph indicated that the majority of the pellets were located in the large intestine.10 McKinney2 reported a BLL of 57 µg/dL for a 5-year-old child 13 hours after ingestion of lead pellets from a strap-on ankle weight. Two unpublished case reports from the Oregon Childhood Lead Poisoning Prevention Program noted similar findings. The first patient was a 10-year-old child who swallowed a fishing weight and exhibited a BLL of 40 µg/dL 3 hours after ingestion. The second patient was a 4-year-old child who swallowed lead shot and exhibited a BLL of 55 µg/dL within 24 hours.

Removal of an LFB located beyond the stomach may include whole-bowel irrigation with a balanced polyethylene glycol solution. Colonoscopic removal should be reserved for objects that remain in the intestine and pose a risk for chronic lead absorption.8 Although it is rare, LFBs can become lodged in the appendix, resulting in appendicitis with or without lead poisoning.6,17

Chelation therapy should be considered in cases with acute BLLs of >45 µg/dL.18 However, controversy exists regarding the timing of chelation. To diminish the risk of enhancing intestinal absorption of lead and increasing the central nervous system penetration of lead, it is recommended that at least 2 doses of dimercaprol be administered intramuscularly before the initiation of EDTA treatment.2 Although efforts should be made to remove the ingested LFB first, the use of chelating agents should not be withheld if endoscopic removal must be delayed and encephalopathy is present.

On the basis of our review of published case reports, it is advisable that all children who ingest metallic foreign bodies undergo BLL testing, which should be repeated within 24 hours if levels are elevated. It may also be prudent to measure BLLs for children with nonmetallic foreign bodies. Wiley et al19 found that children <6 years of age with foreign bodies in the ear, nose, or gastrointestinal tract had higher mean BLLs, compared with control subjects with similar environmental risk factors for lead exposure. This finding suggests that behaviors such as inserting foreign bodies into body orifices represent a risk factor for lead poisoning and children exhibiting these behaviors may require BLL tests. In the case described by McKinney,2 the child passed not only 11 lead pellets but also nonmetallic beads and an eraser.


   CONCLUSIONS
TOP
 ABSTRACT
 CASE REPORT
 DISCUSSION
 CONCLUSIONS
REFERENCES
 
This case report illustrates several important issues. First, it illustrates the presence of lead hazards in objects routinely intended for use by children. Clinicians and caretakers of children should be alerted to the fact that lead can be found in unsuspected objects, and lead poisoning should be considered for any child who ingests a foreign object. All children who ingest metallic foreign bodies should undergo BLL testing, with frequent monitoring. Second, pediatric health care providers should include lead poisoning in the differential diagnosis, particularly when a child is diagnosed with anemia of unknown cause and/or probable gastroenteritis that does not follow the usual course, warranting additional evaluation, including abdominal radiographs and BLL tests. This case report clearly illustrates the critical advocacy role that health care providers can play in identifying hazards affecting children's health and the importance of timely reporting of such hazards to public health authorities, so that appropriate actions can be initiated. The recall that resulted from the reporting of this case likely protected other children from exposure to this lead source.


   ACKNOWLEDGMENTS
 
We acknowledge the following people who provided support in the investigation and follow-up monitoring of this case: Barbara R. Zeal, Marilyn J. Scott, David H. Lew, and Wendy L. Pickner from the Oregon Childhood Lead Poisoning Prevention Program, Oregon Department of Human Services, Oregon Health Services; Daniel W. Peddycord, Elaine Severson, Kathleen M. Moore, and Nadine J. Pusel from the Deschutes County Health Department; M.W. Shannon from Children's Hospital Boston; and A. Jaffe from Oregon Health and Science University.


   FOOTNOTES
 
Accepted Jun 14, 2004.

Reprint requests to (R.D.L.) Oregon Childhood Lead Poisoning Prevention Program, Oregon Department of Human Services, Oregon Health Services, PO Box 14450, Portland, OR 97293-0450. E-mail: richard.d.leiker{at}state.or.us


   REFERENCES
TOP
 ABSTRACT
 CASE REPORT
 DISCUSSION
 CONCLUSIONS
 REFERENCES
 

  1. Watson WA, Litovitz TL, Rodgers GC, et al. 2002 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. 2003;21 :353 –421[CrossRef][ISI][Medline]
  2. McKinney P. Acute elevation of blood lead levels within hours of ingestion of large quantities of lead shot. J Toxicol Clin Toxicol. 2000;38 :435 –440[CrossRef][ISI][Medline]
  3. Greensher J, Mofenson HC, Balakrishnan C, Aleem A. Lead poisoning from ingestion of lead shot. Pediatrics. 1974;54 :641 –642[Abstract/Free Full Text]
  4. Hugelmeyer CD, Moorehead JC, Horenblas L, Bayer MJ. Fatal lead encephalopathy following foreign body ingestion: case report. J Emerg Med. 1988;6 :397 –400[CrossRef][Medline]
  5. Forsby N, Fristedt B, Kjellman B. Acute, lethal poisoning after ingestion of metallic lead. Acta Paediatr Scand. 1967;(suppl 177) :107
  6. Lyons JD, Filston HC. Lead intoxication from a pellet entrapped in the appendix of a child: treatment considerations. J Pediatr Surg. 1994;29 :1618 –1620[CrossRef][ISI][Medline]
  7. Fergusson J, Malecky G, Simpson E. Lead foreign body ingestion in children. J Paediatr Child Health. 1997;33 :542 –544[ISI][Medline]
  8. Mowad E, Haddad I, Gemmel DJ. Management of lead poisoning from ingested fishing sinkers. Arch Pediatr Adolesc Med. 1998;152 :485 –488[Abstract/Free Full Text]
  9. Esernio-Jenssen D, Donatelli-Guagenti A, Mofenson HC. Severe lead poisoning from an imported clothing accessory: "watch" out for lead. J Toxicol Clin Toxicol. 1996;34 :329 –333[ISI][Medline]
  10. Treble RG, Thompson TS. Elevated blood lead levels resulting from the ingestion of air rifle pellets. J Anal Toxicol. 2002;26 :370 –373[ISI][Medline]
  11. Frederick M, Beihusen C, Pulanski EJ. Lead poisoning after ingestion of a foreign body retained in the stomach. N Engl J Med. 1956;254 :1179 –1181
  12. Agency for Toxic Substances and Disease Registry. Case Studies in Environmental Medicine: Lead Toxicity. Atlanta, GA: Agency for Toxic Substances and Disease Registry; 2000. Course SS3059
  13. Canfield RL, Henderson CR, Cory-Slechta DA, Cox C, Jusko TA, Lanphear B. Intellectual impairment in children with blood lead concentrations below 10 µg per deciliter. N Engl J Med. 2003;348 :1517 –1526[Abstract/Free Full Text]
  14. Centers for Disease Control and Prevention. Managing Elevated Blood Lead Levels Among Children: Recommendations From the Advisory Committee on Childhood Lead Poisoning Prevention. Atlanta, GA: Centers for Disease Control and Prevention; 2002
  15. Trope I, Lopez-Villegas D, Cecil KM, Lenkinski RE. Exposure to lead appears to selectively alter metabolism of cortical gray matter. Pediatrics. 2001;107 :1437 –1442[Abstract/Free Full Text]
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PEDIATRICS (ISSN 1098-4275). ©2004 by the American Academy of Pediatrics



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