Higher toxicity of ingested metallic lead in a toddler compared to an adolescent

Non‐occupational sources of lead ingestion may include lead objects, historical ceramics, or old paints. Lead is a cumulative poison with a long elimination half‐life of 5–10 years, due to absorption in the bones, where it replaces calcium. Therefore, the intoxication is typically subacute or chronic with anemia, vomiting, constipation, and saturnine colic. In children, due to their less‐resistant blood–brain barrier, also lower intellectual quotient may occur. ¹ , ²

Here we present images documenting ingested lead objects in two patients and a rapid lead absorption in a toddler. Data of two patients who ingested metallic lead objects, the time of their elimination from the gastrointestinal tract (GIT), blood lead level (BLL), hematological and biochemical findings were searched. Finally, the differences in dose and duration of chelation treatment were compared.

Required informed consent has been given for both subjects prior to their inclusion in the study.

A 14‐month‐old boy, with body weight (b.w.) 9.8 kg, accidentally swallowed a round metal historical coin, found by his father 1 h earlier in the forest in August 2020. X‐ray on the same day revealed it in the stomach (Figure 1a). The boy was monitored, and his stool checked, according to European Society of Gastrointestinal Endoscopy Guidelines, which recommend removal if the object is >2.5 cm in diameter. ³

FIGURE 1.

Images concerning the toddler. (a) Lead seal in his stomach. (b) Lead seal removed from stomach 8 days later. (c) Borderline metaphyseal changes on the knees 19 days after Pb seal ingestion excluding chronic Pb intoxication. (d) “Lead lines” on toddler's tibial and fibular metaphyses 4 months after ingestion confirming lead deposit.

On day 7, abdominal colic appeared, followed by vomiting, constipation, and lethargy. He had anemia with basophilic stippling (Hb 91 g/L, normal range [N] 105–135; Hct 29%, N 33–39), elevated bilirubin (28.6 μmol/L, N 2.0–21.0) and liver enzymes' activity (ALT 9.73 μkat/L, N 0.26–0.6; AST 8.61 μkat/L, N 0.2–0.63). The next day, oesophagogastroscopy was performed and a historical lead seal for a miller's sack (18 g), sized 2.4 × 2.0 × 0.4 cm (Figure 1b) was removed. BLL on day 9 after ingestion was 1174 μg/L. ⁴

Chelation with succimer was started 12 days after ingestion. X‐ray of the knees 19 days after ingestion of Pb described only borderline metaphyseal changes (Figure 1c), clinical symptoms diminished and BLL dropped to 365 μg/L. In September 2020, BLL increased to 436 μg/L and a second DMSA course was given; BLL then decreased to 334 μg/L. A third identical course was given in November, when BLL reached 429 μg/L. At this time, anemia improved slightly (Hb 95 g/L; Hct 31%).

In December 2020, a fourth DMSA course was given, as BLL increased to 487 μg/L. X‐ray of the knees showed “lead lines”, that is metaphyseal bands, typical for chronic lead intoxications (Figure 1d). Neurological examination including electroencephalography showed no abnormalities.

To exclude lead exposure from domestic sources, BLLs in parents and two brothers were measured (13.0–19.8 μg/L). Additional X‐ray in January 2021 excluded metallic objects in toddler's GIT.

Fourteen months after ingestion, BLL was still 317 μg/L. Finally, two DMSA courses were given in November and December 2021, and the lowest BLL of 107 μg/L was reached. Three years after ingestion, his BLL was 197 μg/L and health condition was good with normal psychomotor development and growth.

A 17‐year‐old girl, body weight (b.w.) 55 kg, with mental anorexia ingested ‐ to lower her appetite ‐ within 5 min 500 lead shot (245 g Pb) for airguns for hunting small wild animals. Five weeks later, when she had intense GIT symptoms, X‐ray revealed a huge mass of lead shot in her stomach (Figure 2a). Her BLL 6 weeks after ingestion reached 1100 μg/L. She had anemia with basophilic stippling (Hb 82 g/L, N 120–165; Hct 24.2%, N 33–47). Bilirubin (76.2 μmol/L, N 4.0–24.0) and liver enzymes were elevated (ALT 12.7 μkat/L, N 0.15–0.96; AST 8.54 μkat/L, N 0.22–0.87), but serum Fe was normal. After a high‐residue diet, the lead shot was eliminated (Figure 2b) within 3 weeks. She was treated for 13 days using calcium disodium ethylenediamine tetra acetic acid (EDTA; 1.9 g) or oral meso‐2,3‐dimercaptosuccinic acid (DMSA; 20 or 30 mg/kg/day). Three months later, one EDTA infusion decreased BLL from 600 μg/L to 340 μg/L.

FIGURE 2.

Radiographs of the adolescent. (a) Lead shot in the stomach 5 weeks after ingestion. (b) Lead shot in the gastrointestinal tract of the adolescent after high‐residue diet 6 weeks after ingestion.

During the past 20 years, we treated 12 subjects with subacute 5–12 weeks´ oral exposures, including two sisters exposed to residues from lead paint who received two DMSA courses. BLL of the 5‐year‐old girl dropped within 6 months from 356 μg/L to 72 μg/L and that of her sister 2–1/2 years old went from 240 to 48 μg/L. ⁵

Solely the toddler's ingestion of a lead seal led to recurring high BLL and a need for six 19–24 days' series of chelating treatment within 18 months.

This difference may be explained by a higher oral lead absorption in very young children, as great as 40% compared with 10%–15% in adults, as well as diminished activity of ALA‐dehydratase and accumulation of free protoporphyrin in erythrocytes already at 200 μg/L in children but at 250–300 μg/L in adults. ⁶ The acidity of gastric juice, containing HCl, favors dissolution of lead, and in the proximal duodenum, the principle absorption of Pb occurs. Developing intestinal mechanisms in small children can lead to increased absorption of lead; in addition, drinking milk and earlier fasting may increase Pb absorption. ⁷ A variation in individual susceptibility, due to a genetic polymorphism, including ALA‐dehydratase may also play a role. ¹ , ⁶ , ⁷

Such a rapid elevation of BLL has been observed in children. For example, a girl 5 1/2 years old ingested thousands of small Pb pellets. Within a few hours after hospital admission, she had BLL 570 μg/L, and a normal blood count, which decreased only 5 days later. ⁸

BLLs associated with fatalities fall mostly into the range 1110–3500 μg/L. Two lethal cases are reported of 2‐year‐old girls dying due to encephalopathy after ingesting lead curtain weights. The first object (diameter 22 mm) persisted in the stomach for an unknown time. ⁹ The second object (20 × 30 mm) remained for 6–8 weeks and pre‐mortem BLL was 2830 μg/L. ¹⁰

In our two patients, different chelating antidotes were used, but that does not explain the persistence of high BLL in the child, as succimer produces greater urinary lead excretion than does EDTA. ²

Despite its removal by endoscopy after 1 week, ingestion of a lead object by a 14‐month‐old boy led to very high BLL and development of severe symptoms, including bone absorption.

Although the 17‐year‐old girl ingested 4.45 g lead/kg b.w. and the toddler only 1.83 g/kg b.w., he required repeated chelation over 1.5 years.

Main reason of the severity in the toddler's case appears the more rapid lead absorption and a higher individual sensitivity, as environmental contamination with lead was excluded.

In small children, immediate removal of lead objects from the stomach is crucial. In the event of a suspicious X‐ray images of unknown metallic objects, BLL should be tested within hours.

AUTHOR CONTRIBUTIONS

DP, JP, and SA designed the manuscript, PJ critically reviewed the manuscript, and all authors read and approved the final manuscript.

INFORMED CONSENT

Informed consent for the publication of this report was obtained from the toddler's parents and from the adolescent' patient.

CONFLICT OF INTEREST STATEMENT

The authors declare no conflicts of interest.

Pelclova D, Jabandziev P, Aulicka S, Papez J. Higher toxicity of ingested metallic lead in a toddler compared to an adolescent. Pediatr Int. 2025;67:e70039. 10.1111/ped.70039