Lead exposure during demolition of a steel structure coated with lead-based paints. II. Reversible changes in the conduction velocity of the motor nerves in transiently exposed workers.

Lead exposure during demolition of a steel structure coated with lead-based paints: II Reversible changes in the conduction velocity of the motor nerves in transiently exposed workers. Scand J Work Environ Health 13(1987)56-61. In a group of workers exposed to high levels of lead during five months nerve conduction velocity parameters were evaluated at the termination of exposure, and also three and fifteen months later. At the termination of exposure the mean blood lead level was 4.0 "mol/I, and motor conduction velocities in the median and the ulnar nerves were slower and the distal latencies in the median nerve were longer compared to the values measured 15 months later. Sensory conduction velocities, measured distally in the same nerves, were not depressed compared to the values measured three or fifteen months later. It was tentatively con cluded that the effect of lead on the conduction velocity of the motor nerves has an initial reversible phase, dependent on the duration of exposure.

The toxic effect of chronic exposure to lead on the peripheral nervous system in man has been studied extensively in epidemiologic investigations (2,3,4,5,6,8,10,II,12,13,14,15,16,17,18,20). On the basis of such investigations it is generally agreed that chronic exposure to lead can reduce the conduction velocity of the fastest fibers in the motor nerves in both the arms and legs, although some disagreement persists about the minimum level of lead exposure leading to such an effect.
Investigations on the effects of transitory exposure to lead on the peripheral nervous system are scarce. To the best of our knowledge only studies tangentially connected to this subject have been published. (See references 1,7 and 9). In a recent study, Spee & Zwennis (19) reported that workers involved in the demolition of a large steel bridge showed a sharp rise in blood lead levels. Thus it was decided to evaluat e the peripheral nerve conduction of these workers. The present report describes the results of these measurements.

Demolition workers
The bridge was demolished by a working party composed of eight men. Initially the party was assisted by I  56 a ninth worker, number 8 in the paper of Spee & Zwennis (19), but only for a short period, and that particular worker was therefore not included in the study. All eight consented to take part in the investigation. The mean age was 38.6 (SD 8.1) years. (See table 3 in the Results section.) Exposure to lead originated from the lead-based paint which was burnt in the process of cutting the bridge into parts. The demolition of the bridge, and thus the exposure to lead , lasted five months. Towards the completion of the hob two workers complained about gastrointestinal symptoms indicative of lead intoxication. Further details regarding exposure have been presented by Spee & Zwennis (19).

Referents
Nine volunteers (male laboratory workers) comprised a reference group. They were not occupationally exposed to lead nor did they suffer from any known diseases predisposing to peripheral neuropathy. The mean and standard deviation of age in the reference group, 38.3 years and 8.0 years, respectively (table I), were similar to those of the lead-exposed group .

Electrophysiology
The nerve conduction velocity of the fastest motor fibers of the median and ulnar nerves were measured from the elbow to the wrist. The distal motor latencies of both nerves were recorded as well. In addition the,conduction velocity of the fastest sensory fibers of the median and ulnar nerves was measured antidromically from the wrist to the ring finger. Convention-al methods, using skin electrodes, were employed. The nerves were stimulated with constant current pulses from a unit (IS/C, Medelec) triggered by the electromyograph (MS 91, Medelec). Conduction velocity parameters are dependent on the temperature. of the nerves. When the skin temperature is above 30°C on the lower arm and above 27°C on fingertips , however, conduction velocity parameters are not dependent on skin temperature (17). Ashby (2) gives slightly higher values, above 31°C at the wrist and above 33°C at the elbow. To assure this condition, the hand was warmed up to the wrist in water of 39°C for 3 min before the measurement. During the measurement the hand and the lower arm were prevented from cooling by the heat delivered by two infrared heaters .

Blood lead levels
The blood lead conten t was determined by atomic absorption spectrophotometry. For furt her deta ils the reader is referred to the report of Spee & Zwennis (19).

Design of the experiment
Nerve conduction velocity was monitored at the termination of exposure and at three and fifteen months postexposure. Preexposure values were not available . Since the number of people was rather small for the detection of changes in a comparison with a reference gro up, only longitudinal comparisons within the exposed group were carried out. In addition the stability of the nerve conduction velocity parameters over time was investigated. Therefore, the nerve conduction velocities of the subjects in the reference group were measure d twice with an interval of one year. The Wilcoxon signed rank test (two-tailed, p<0.05) was used to evaluate the significance of the results . A distribution-free test was used because exposure was not the same for each worker, so that, at least in prin-ciple, violation of the normality of the distribution of the parameters could be expected.

Unexposed reference group
The individual results and the mean values of the nerve conduction velocities measured on the first occasion in the unexposed reference group are presented in table I . Moreover the value at which a detor iation deviates by 2 SO units from the mean value is given for each parameter. Only one value exceeded these limits . One year later (table 2) four values exceeded these limits. Except for the sensory conduction velocity of the median nerve no statistically significant differences emerged in the two series.

Workers exposed to lead
The number of individual values exceeding the limits, as determined by the measurements of the reference group, decreased in the group exposed to lead after the exposure , ie, there were I I at the termination of exposure (table 3), six at three months after the termination (table 4) and five at 15 months after the termination (table 5). A comparison between the values obtained at the termination of exposure (table 3) and three months later (table 4) did not show any significant differences with regard to the conduction velocity parameters. However, a comparison between the values obtained at the term ination of exposure (tab le 3) and 15 mont hs later (table 5) revealed a statistically significant increase in the cond uction velocity of the motor fibers of the median and ulnar nerves, being 2.8 and 3.4 m/s, respectively, and a significant decrease (which is also an improvement) in the distal latency of the median nerve (by 0.37 ms). Significant changes in the sensory conduction velocity of the median and ulnar nerves and in the dista l motor latency of the ul-  Table 3. Individual values and the means of the conduction veloc ities and distal latencies of t he lead-exposed workers, measured at the term ination of exposure. The values in ita lics deviate by more than 2 SD un its f rom the reference means (tab le 1).  Ind ividual values and the means of the conduction veloc ities and distal latencies of the lead-exposed workers, measured 15 months after the termination of exposure. The values in itali cs deviate by more than 2 SD units fr om the refere nce means (

Discussi on
With regard to the results of the exposed worker s, it was found that 15 months aft er the termination of exposure the conduction velocities of the fastest motor fibers of the median and ulnar nerves and the distal motor latency of the median nerve had improved in comparison with the values obtained immediately after the termination of exposure. An obvious interpretation is that , because of exposure to lead , the conduction velocities deteriorated and that, in the following period without exposure , the values returned to normal. However, the existence of a small irreversible change cannot be excluded. On the basis of the data reported by Corsi et al (7), obtained in a group of seven patients formerly intoxicated with lead for less than three and a half months, such an irreversible change cannot be excluded either . Yet both in the results of Corsi et al (7) and in the present results (table  2 and table 5) the mean values of the workers, long after the termination of exposure , and tho se of the referents are strikingly smilar. These similarities should not simply be dismissed, but should be taken instead as a hint that an irreversible effect of transitory exposure is less likely. Interesti'ngly, in a different group of patients exposed to lead for at least six months, Corsi et al (7) could still demonstrate a significant motor cond uction deficit after exposure had been terminated for at least three years and lead had been removed by chelation from the body at least two years before the measurement. The deficit was 4.9 ml s and 3.8 mls in the ulnar and peroneal nerves, respectively.
It can tentatively be concluded that the toxic effect of lead on the peripheral nervous system has two phases possibly caused by different mechanisms. Exposure to lead during less than a few months leads to an at least partly, if not completely, reversible decrease in motor conduction velocity. However, exposure to lead for at least six months can lead to a permanent decrease in motor conduction velocity.
Araki et al (1) have reported that chelat ion therapy leads to an increase of the nerve conduction velocity in some, but not all, patients with lead intoxication. In most cases the increase in the conduction velocity was recorded within a month after chelation. It can be inferred that, if a decrease in the nerve conduction velocity due to exposure to lead can be reversed, the reverse is rather fast. It seems plausible that the delay found in the improvement of the nerve conduction velocity in the present study was simply due to the time course of the removal of lead from the body, rather than it being associated with structural repair in the nerves.
Feldman et al (9) have investigated workers dismantling an elevated train network. Because of the burning of lead-based paint, the blood lead content increased to a mean of 4.0 /tmol/I in 32 burner workers and to a mean of 2.4/tmol/l in 12 nonburner workers. A mean decrease of 5.8 mls was found in the motor conduction velocity of the peroneal nerve in a comparison of 13 burner workers with six nonburner workers. The decrease was larger than the changes found in the present study for the motor fibers of the median (2.8 mls) and ulnar (3.4 mls) nerves. Feldman et al (9) did not state clearly how long exposure lasted; however the authors did report that symptoms of increased bodyburden appeared for lead after a period of exposure as short as one month. Workers with such symptoms were chelated. Unfortunately Feldman et al (9) did not report on the recovery of the nerve conduction velocity after chelation nor after the termination of exposure.
The reproducibility of the motor conduction velocity parameters and the distal sensory conduction velocity of the ulnar nerve in the reference group was satisfactory, ie, the differences were not significant. However the reproducibility of the distal sensory conduction velocity of the median nerve was poor in that a statistically significant difference existed. The lack of a difference in the other distal parameters indicates that a difference in temperature of the hand can be ruled out as a cause. Except chance , no other cause seems present.
In our experiment the distal conduction velocity of the sensory fibers did not increase in the recovery period after the short-term, but relatively high exposure. (The biological limit recommended for blood lead content by the countries of the European common market is 3.4 /tmol/I.) Singer et al (18) found that, in a group of workers exposed to lead for less than 10 years, only a decrease in the (distal) conduction velocity of the sensory nerves could be found, whereas in a group of workers in the same factory, exposed longer than 10 years, a decrease in the conduction velocity of the motor nerves could be demonstrated as well. Such findings suggest that a decrease in conduction velocity develops earlier in sensory fibers than in motor fibers. Seppalainen et al (17) also found evidence supporting this possibility. Our results indicate that a reversible decrease in the distal conduction velocity of the sensory nerves after exposure to lead during months 60 rather than years cannot be demonstrated at all, but a limited irreversible decrease cannot be excluded.
It might be contended that the present result, ie, a transitory decrease in motor conduction velocity in the exposed workers, was caused by a difference in the mean temperature of the upper extremities at the time of the subsequent measurements. However the absence of a change in the distal sensory conduction velocity does not support such a contention.
In conclusion, it was found that after the termination of a transitory exposure to lead the motor conduction velocity and the distal motor latency, but not the distal sensory conduction velocity, improved in the workers involved. It was argued that a reversible component was present in the decrease of motor conduction velocity resulting from transitory exposure to lead and that sensory conduction velocity is probably not affected under these conditions.