been raised regarding the potential of lead toxicity to occur from mobilization of these bone stores during times of increased bone turnover, such as pregnancy, lactation, and other hypermetabolic states [Silbergeld, 1991]. We describe the presentation, evaluation, and treatment of a patient with lead poisoning, no identifiable ongoing lead exposure, high skeletal lead as noted by K-X-ray fluorescence (K-XRF, an in vivo method of accurately quantitating bone stores), and marked hyperthyroidism.
Initial presentation. A 37-year-old woman employed as a salesperson in a clothing store experienced persistent fatigue, insomnia, difficult concentrating, abdominal cramps, weight loss, muscle and joint aching, and tremor for several months. After reading newspaper reports on lead poisoning, she wondered if her symptoms might be related to work she last performed 7 years earlier, when she removed paint during the course of renovating houses. She requested a blood lead tests from an otolaryngologist who was treating her for an ear infection. The physician found that her chemistry screen (glucose, liver function tests, blood urea nitrogen, creatinine, calcium, and phosphorus) was normal, but that she had an elevated blood lead level of 2.46 µmol/l (51 µg/dl) and an elevated erythrocyte protoporphyrin (EP) level of 0.78 µmol/l (44 µg/dl; normal <0.62 µmol/l or 35 µg/dl).
She was referred to an occupational medicine specialist (R.H.G.). Detailed questioning did not reveal any sources of recent lead exposure. Her two teenage children who lived with her were asymptomatic and had blood leads less than .19 µmol/l (4 µg/dl).
Seven and 10 years previously she had assisted with the deleading of two homes. For a total of about 6 months she scraped and sanded lead paint, wore no respiratory protection, and smoked and ate at the work site. She also recalled that as a child she lived in an old house, frequently chewed on woodwork, windowsills, paper, and pencils, and had chronic abdominal complaints and anemia. She did not recall having a blood lead test as a child. She was held back for 1 year in school because of “math problems.”
Her medical history was notable only for symptoms of Raynaud’s phenomenon, for which she briefly had taken verapamil without relief. She smoked one pack of cigarettes daily and denied any regular alcohol ingestion.
On physical examination she appeared clinically hyperthyroid, with a regular pulse of 112, blood pressure of 130/60 mm Hg, diffusely enlarged and tender thyroid gland, marked “lid lag,” fine resting tremor of both hands, and symmetric hyperreflexia. She also had difficulty replicating Bender diagrams.
The blood lead level, which was measured by flameless atomic absorption spectroscopy in an OSHA-approved laboratory (Bioran, Inc.), was 2.56 µmol/l (53 µg/dl). The EP level, which was measured by hematofluorometry (ESA Labs, Inc.), was 0.66 µmol/1 (38 µg/dl). The serum thyroxine (T4) was >257 nmol/l (>20 µg/dl; normal 64–154 nmol/l), the triiodothyroxine (T3) uptake was 39.9% (normal 30– 40%), free thyroxine (free T4) was 108 pmol/l (8.4 ng/dl; normal 9.0–22), and thyroxine stimulating hormone was (TSH) <0.05 mIU/l (normal 0.46–3.59). The blood urea nitrogen was 6.1 mmol/l (17 mg/dl), and the serum creatinine 61.9 µmol/l (0.7 mg/dl). The hematocrit was 39.6% and the hemoglobin was 133 g/l (13.3 g/dl). No basophilic stippling was seen on a blood smear. A 24-hour radioactive iodine