ABSTRACT Twenty lead-exposed men were selected on the basis of a maximum level of lead in the blood of 70-140 μg/100 ml within the past year. There was no clinical evidence of neuropathy attributable to lead and haemoglobin levels were normal. In individuals, maximum motor and sensory conduction and the amplitude of the evoked potentials were normal or borderline in the median, peroneal and sural nerves, except in the distal portion of the deep peroneal nerve. In this nerve, motor conduction was slowed because of compression by metal-lined safety shoes; changes in this segment are not included in the findings. When the average conduction velocity in lead-exposed men was compared with the average in nerves of controls matched for age, distal motor latency was slightly prolonged in the median nerve. The average latency for proximal muscle supplied by the peroneal nerve was prolonged, and the maximum motor conduction velocity was slowed in the median nerve from elbow to wrist (0·01 > p <0·001). In addition, the average maximum sensory conduction was slightly slowed along the distal and intermediate portion of the superficial peroneal and sural nerves (p <0·001). The average minimum sensory conduction velocities were normal, as were the average amplitudes of the evoked muscle action potentials and the average ratio of amplitude of the muscle action potential evoked by stimuli at a proximal and a distal nerve site. The average amplitude of the sensory potentials recorded in the median and the superficial peroneal nerves tended to be increased. Electromyography of the abductor pollicis brevis and anterior tibial muscles showed that the only abnormality was an increased incidence of polyphasic potentials in the anterior tibial muscle of seven men. Neither the slowing in conduction nor the histological findings in the sural nerves of eight men were related to the level of lead in the blood. The slight slowing in conduction suggests a minor defect in the excitable membrane of the nerve fibre: it was not attributable to histological abnormalities in the sural nerve, in which the number of myelinated and unmyelinated nerve fibres was normal and demyelination was absent. In teased fibres, those with paranodal remyelination were slightly increased, and few fibres had segments with diminished diameter. The mechanism of the defect causing the slight slowing in conduction in lead-exposed men seems to differ from the lesion in patients with clinical evidence of lead neuropathy, which is axonal in type. It is, therefore, doubtful whether the slight slowing in the nerves of the group of lead-exposed men should be classified as a subclinical neuropathy.
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