Case Studies in Toxicology: Drink the Water, but Don’t Eat the Paint
The young pediatric central nervous system (CNS) is much more vulnerable to the effects of lead than the adult CNS. Even low-level lead exposure to the developing brain causes deficits in intelligence quotient, attention, impulse control, and other neurocognitive functions that are largely irreversible.7
Children with an elevated BLL may also develop constipation, anorexia, pallor, and pica.8 The development of geophagia (subtype of pica in which one craves and ingests nonfood clay or soil-like materials), represents a “chicken-or-egg” phenomena as it both causes and results from lead poisoning.
Lead impairs multiple steps of the heme synthesis pathway, causing microcytic anemia with basophilic stippling. Lead-induced anemia exacerbates pica as anemic patients are more likely to eat leaded paint chips and other lead-containing materials such as pottery.8 Of note, leaded white paint is reported to have a pleasant taste due to the sweet-tasting lead acetate used as a pigment.
The most dramatic and consequential manifestation of lead poisoning is lead encephalopathy. This can occur at any age, but manifests in children at much lower BLLs than in adults. Patients can be altered or obtunded, have convulsive activity, and may develop cerebral edema. Encephalopathy is a life-threatening emergency and must be recognized and treated immediately. Lead encephalopathy should be suspected in any young child with hand-to-mouth behavior who has any of the above environmental risk factors.4 The findings of anemia or the other diagnostic signs described below are too unreliable and take too long to be truly helpful in making the diagnosis.
How is the diagnosis of lead poisoning made?
The gold standard for the diagnosis of lead poisoning is the measurement of BLL. However, the turnaround time for this test is usually at least 24 hours, but may take up to several days. As such, adjunctive testing can accelerate obtaining a diagnosis. A complete blood count (CBC) to evaluate for microcytic anemia may demonstrate a characteristic pattern of basophilic stippling.9 A protoporphyrin level—either a free erythrocyte protoporphyrin (FEP) or a zinc protoporphyrin level—will be elevated, a result of heme synthesis disruption.9 Urinalysis may demonstrate glycosuria or proteinuria.6 Hypertension is often present, even in pediatric patients.
An abdominal radiograph is essential in children to determine whether a lead foreign body, such as a paint chip, is present in the intestinal lumen. Long bone films may demonstrate “lead lines” at the metaphysis, which in fact do not reflect lead itself but abnormal calcium deposition in growing bone due to lead’s interference with bone remodeling. A computed tomography (CT) scan of the brain in patients with encephalopathy will often demonstrate cerebral edema.6
Of note, capillary BLLs taken via finger-stick can be falsely elevated due contamination during collection (eg, the presence of lead dust on the skin). However, this screening method is often used by clinicians in the pediatric primary care setting because of its feasibility. Elevated BLLs from capillary testing should always be followed by a BLL obtained by venipuncture.2
Case Continuation
The patient’s mother was counseled on sources of lead contamination. She was informed that although drinking water may contribute some amount to an elevated BLL, the most likely source of contamination is still lead paint found in older homes such as the one in which she and her son resided.
Diagnostic studies to support the diagnosis of lead poisoning were performed. A CBC revealed a hemoglobin of 9.8 g/dL with a mean corpuscular volume of 68 fL. A microscopic smear of blood demonstrated basophilic stippling of red blood cells. An FEP level was 386 mcg/dL. An abdominal radiograph demonstrated small radiopacities throughout the large intestine, without obstruction, which was suggestive of ingested lead paint chips.
What is the best management approach to patients with suspected lead poisoning?
The first-line treatment for patients with lead poisoning is removal from the exposure source, which first and foremost requires identification of the hazard through careful history taking and scene investigation by the local health department. This will avoid recurrent visits following successful chelation for repeat exposure to an unidentified source. Relocation to another dwelling will often be required for patients with presumed exposure until the hazard can be identified and abated.
Patients who have ingested or have embedded leaded foreign bodies will require removal via whole bowel irrigation or surgical means.
Following decontamination, chelation is required for children with a BLL more than 45 mcg/dL, and adults with CNS symptomatology and a BLL more than 70 mcg/dL. Table 2 provides guidelines for chelation therapy based on BLL.5
There are three chelating agents commonly used to reduce the body lead burden (Table 2).5 The most common, owing largely to it being the only agent used orally, is succimer (or dimercaptosuccinic acid, DMSA). The second agent is calcium disodium edetate (CaNa2EDTA), which is given intravenously. In patients with encephalopathy, EDTA should be given after the first dose of the third agent, British anti-Lewisite (BAL; 2,3-dimercaptopropanol), in order to prevent redistribution of lead from the peripheral compartment into the CNS.10 However, BAL is the most difficult of the three agents to administer as it is suspended in peanut oil and is given via intramuscular injection every 4 hours.
Unfortunately, while chelation therapy is highly beneficial for patients with severe lead poisoning, it has not been demonstrated to positively impact children who already have developed neurocognitive sequelae associated with lower level lead exposure.11 This highlights the importance of prevention.
