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A neurological and biochemical study of early lead poisoning
  1. Judith A S Ashby
  1. 1Department of Occupational Health, University of Manchester, Manchester M13 9PT, UK

    Abstract

    ABSTRACT Changes in nerve conduction velocity were found in 94 workers exposed to lead in a battery factory compared with 94 age-matched controls. There was no clinical evidence of nerve damage in the lead workers. The mean blood lead concentration in the 94 lead workers was 2·9 μmol/l (60 μg/100 ml) and their length of exposure to lead ranged from 6 months to 33 years.

    All mean maximum motor nerve conduction velocities (MMCV) measured were highly statistically significantly lower in the lead-exposed group when compared with their age-matched controls. Thus mean ulnar MMCV was 53·4 m/s in lead workers and 55·6 m/s in control subjects (p < 0·0005); mean median MMCV was 55·9 m/s in lead workers and 57·3 m/s in control subjects (p < 0·01); mean radial MMCV was 63·9 m/s in lead workers and 71·1 m/s in control subjects (p < 0·0005); mean peroneal MMCV was 46·1 m/s in lead workers and 47·6 m/s in control subjects (p < 0·005).

    The amplitude of the muscle action potential produced by proximal stimulation of a nerve was expressed as a percentage of the amplitude of the muscle action potential produced by distal stimulation and the percentage amplitude thus obtained used as an indicator of the conduction velocity of slower fibres (SFCV). Peroneal nerve percentage amplitude of lead workers was statistically significantly lower (p < 0·005) than in the control group (means 86·6% and 90·3% respectively). There were, however, no significant differences in the percentage amplitude in the ulnar and median nerves. It is suggested that percentage amplitude is an inappropriate indicator of SFCV in ulnar and median nerves.

    There was no statistically significant correlation to indicate that progressive slowing of nerve conduction (MMCV and SFCV) was associated with increasing exposure to lead (as indicated by blood and urine lead concentrations) or with the commonly measured biochemical changes associated with disturbed haemopoiesis in lead exposure (δ-aminolaevulinic acid dehydrase; free erythrocytc protoporphyrin; haemoglobin and urinary δ-aminolaevulinic acid). MMCV of the ulnar nerve was the only conduction velocity statistically significantly correlated with length of exposure to lead. Increased length of exposure to lead was associated with a decrease in the ulnar MMCV.

    Only 13 of the subjects had been exposed to lead for two years or less and in none of them had the blood lead ever risen above 3·9 μmol/l (80 μg/100 ml) in three-monthly tests (mean blood lead concentration at time of testing: 2·8 μmol/l). In these subjects the MMCV of ulnar, radial, and peroneal nerves and the peroneal percentage amplitude were statistically significantly reduced. The results from this group suggest that the onset of nerve conduction changes occurs within two years and at concentrations of lead in blood of less than 3·9 μmol/l (80 μg/100 ml).

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