Discussion

This case demonstrates that clinically significant lead poisoning may occur in completely asymptomatic children. Reliance on symptoms may delay diagnosis, allowing for progression of toxicity. In this case, the patient was identified before developing clinical manifestations, highlighting the value of screening based on risk factors rather than symptoms alone. In this patient, several recognised risk factors were present: pica, iron-deficiency anaemia, and developmentally appropriate hand-to-mouth behaviours. Together, these factors prompted blood lead level screening despite the absence of symptoms and ultimately led to early diagnosis. This is particularly important because there is no recognised safe blood lead concentration in children, and adverse neurodevelopmental effects have been demonstrated even at relatively low levels. Early identification before the onset of symptoms is thus essential to minimise the risk of irreversible neurodevelopmental injury.

Pica substantially increases the likelihood of ingesting lead-containing materials. Common sources include peeling paint from the walls, plaster, soil, and dust. Although lead-based household paint has been banned in the UK since 1992 [4], legacy paint remains an important source of childhood exposure. In this case, ingestion of paint was considered the most likely source of lead, although the precise age and origin of the paint could not be confirmed. Similar cases have been reported. For example, a 2016 case report [5] by Jouhadi et al described lead poisoning secondary to pica, reinforcing the importance of screening children with recognised risk factors.

The presence of iron deficiency anaemia in this case is also pertinent given the link between iron deficiency and lead absorption. As both metals share some transport pathways, absorption of lead is increased in iron deficiency, rendering these patients more susceptible to lead toxicity [6]. It is therefore vital that iron deficiency be corrected promptly, whether through oral or intravenous replacement; in this case, the patient started oral iron replacement early on in their clinical course. Iron deficiency is therefore an important modifiable risk factor for lead toxicity.

Chelation therapy utilised in this case was indicated due to the markedly elevated blood lead levels. Chelators work by forming tight chemical bonds with heavy metals, thereby enabling them to be excreted. Although effective in reducing circulating lead, it does not remove lead stored within bone, meaning blood lead concentrations may rebound following treatment. In this patient’s case, her levels stagnated at 1.60 μmol/L in her most recent follow-up (see Table 4), which may reflect redistribution of lead from skeletal stores following chelation therapy, although continued environmental exposure must be excluded. Ongoing surveillance of lead levels is therefore essential.

Perhaps the most important learning point from this case is that chelation alone is insufficient if the environmental source of exposure is not identified and eliminated. It is compulsory to report all cases of lead poisoning levels ≥ 0.24 μmol/L to relevant public health authorities, who then carry out investigations to identify the lead source [7]. Without these steps, blood lead levels may continue rising, and repeated chelation therapy may become necessary. In this case, although the paint seems the likely source of lead toxicity, it is only through thorough investigations and routine blood lead levels during follow-ups that we can assure the source has been identified and removed successfully, reducing the risk of ongoing or recurrent exposure.

This case highlights that targeted blood lead level screening in children with pica, iron-deficiency anaemia and other recognised risk factors can facilitate early diagnosis and treatment before the development of irreversible neurodevelopmental sequelae.