Subclinical cervico-spino-bulbar effects of lead: a study of short-latency somatosensory evoked potentials in workers exposed to lead, zinc, and copper
- PMID: 3019134
- DOI: 10.1002/ajim.4700100207
Subclinical cervico-spino-bulbar effects of lead: a study of short-latency somatosensory evoked potentials in workers exposed to lead, zinc, and copper
Abstract
Subclinical central and peripheral nervous system dysfunction among lead-exposed workers was studied by measuring short-latency somatosensory evoked potentials (SSEP) and maximal motor and sensory nerve conduction velocities (MCV and SCV) following stimulation of the median nerve at the wrist. The examinations were conducted in 20 gun-metal foundry workers exposed to lead, zinc, copper, and tin, with blood lead (BPb) concentrations of 16 to 64 micrograms/dl (mean, 42 micrograms/dl). The interpeak latency of SSEP in the cervico-spino-bulbar region [N9(Erb)-N13 latency] was significantly prolonged, and the MCV and SCV in the forearm were significantly slowed. Multiple regression analysis revealed that the yield of urinary lead following challenge with calcium disodium ethylenediamine tetraacetate (CaEDTA) and packed red blood cell volume were the major factors associated with the prolongation of SSEP latency in the cervico-spino-bulbar region. Similarly, the interpeak latency in the upper central nervous system (N13-N20 latency) was inversely related to the zinc concentration in erythrocytes; latency up to the Erb's point [N9(Erb) latency], which reflects conduction time in a long pathway of the sensory median nerve, was inversely related to urinary zinc level; the MCV and SCV in the palm were positively related to erythrocyte zinc concentration and plasma copper concentration, respectively. These findings suggest that the subclinical neurophysiological effects of lead occur not only in peripheral nerves but also in the central nervous system. It appears that zinc antagonizes the central and peripheral neurologic dysfunction caused by lead; similarly, copper antagonizes the peripheral sensory nerve dysfunction.
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