Peripheral neuropathy in chronic occupational inorganic lead exposure: a clinical and electrophysiological study
- aDepartment of Neurology and Neurosurgery, P Stradin's Clinical University Hospital 13 Pilsonu St, Riga, LV-1002, Latvia, bInstitute of Occupational and Environmental Health, Medical Academy of Latvia, Riga, Latvia, cDepartment of Clinical Neurology, University of Oxford, Radcliffe Infirmary, Woodstock Road, Oxford OX2 6HE, UK
- I Logina, Department of Neurology and Neurosurgery, Medical Academy of Latvia, P Stradins Clinical University Hospital, 13 Pilsonu St Riga, LV-1002, Latvia
BACKGROUND AND OBJECTIVES Traditionally the neuromuscular disorder associated with lead poisoning has been purely motor. This study assessed peripheral nerve function clinically and electrophysiologically in 46 patients with neuropathic features out of a total population of 151 workers with raised blood and/or urinary lead concentrations.
RESULTS Average duration of occupational exposure for the neuropathic group ranged from 8–47 years (mean 21.7). Their mean blood lead concentration (SD) was 63.9 (18.3) μg/dl (normal <40), urinary lead 8.6 (3.3) μg/dl (normal<5.0), urinary coproporphyrins 66.7 (38.4) μg/g creatinine (20–80), urinary aminolaevulinic acid 1.54 (0.39) mg/g creatinine (0.5–2.5). All 46 had distal paraesthesiae, pain, impaired pin prick sensation, diminished or absent ankle jerks, and autonomic vasomotor or sudomotor disturbances. Reduced vibration sensation and postural hypotension were present in all 20 studied. None of these 46 patients had motor anormalities. Motor conduction velocity and compound muscle action potential amplitudes were normal, with marginally prolonged distal motor latencies. Sensory nerve action potential amplitudes lay at the lower end of the normal range, and the distal sensory latencies were prolonged. No direct correlation was found between the biochemical variables, and the clinical or electrophysiological data.
CONCLUSIONS One additional patient was seen with shorter term exposure to lead fumes with subacute development of colicky abdominal pain, severe limb weakness, and only minor sensory symptoms. Unlike the patients chronically exposed to lead, he had massively raised porphyrins (aminolaevulinic acid 21 mg/g creatinine, coproporhyrins 2102 μg/g creatinine). Patients with unusually long term inorganic lead exposure showed mild sensory and autonomic neuropathic features rather than the motor neuropathy classically attributed to lead toxicity. It is proposed that the traditional motor syndrome associated with subacute lead poisoning is more likely to be a form of lead induced porphyria rather than a direct neurotoxic effect of lead.