Chronic Lead Toxicity Presenting With Neurologic Decline in an Adult Male

Lead toxicity in adults is uncommon and can present with progressive neurological manifestations that mimic neurodegenerative diseases. We describe the case of a 61-year-old man with a several-year history of worsening gait instability, cognitive decline, dysarthria, and involuntary movements in the setting of persistently elevated blood lead levels. The patient’s symptoms began in late 2023 with balance difficulties and frequent falls, followed by progressive cognitive impairment, personality changes, and a 100 lb unintentional weight loss. His clinical course was further complicated by chronic non-healing wounds and imaging evidence of renal and hepatic scarring. Extensive neurological evaluation, including CT and MRI of the brain and genetic testing for Huntington’s, was unrevealing. The patient was found to have repeatedly elevated blood lead levels, initially in the 30 μg/dL range and later peaking in the 60 μg/dL range, despite cessation of work at the chemical and metal processing facility he had been employed at. Evaluation of potential ongoing sources revealed multiple retained BB fragments in the hand and foot dating back to early adulthood. These were initially considered as possible contributors, but point-of-care testing of the fragments on removal was negative for lead. A fragment in the foot was embedded in the bone and not amenable to removal. Additionally, possible residential exposure was considered, as the patient resided in a mid-20th-century home. He required multiple hospitalizations for progressive neurologic decline and elevated lead levels, during which he received inpatient chelation therapy with succimer. Chelation was associated with partial improvement and modest cognitive stabilization, though his dysarthria and gait ataxia persisted. His outpatient course was complicated by financial barriers that limited sustained chelation therapy, resulting in recurrent elevations of blood lead levels. Ongoing management included serial monitoring of lead levels following chelation, with plans to pursue surgical removal of a retained abdominal wall wire if levels were to rise again, suggesting an endogenous source.