Effects of pesticides on the peripheral and central nervous system in tobacco farmers in Malaysia: studies on peripheral nerve conduction, brain-evoked potentials and computerized posturography

We examined the effects of pesticides on the central and peripheral nervous system in the setting of a tobacco farm at a developing country. Maximal motor and sensory nerve conduction velocities (MCV and SCV, respectively) in the median, sural and tibial nerves, postural sway, and brain-evoked potentials (auditory event-related and visual-evoked potentials) were measured in 80 male tobacco farmers and age- and sex-matched 40 controls in Kelantan, Malaysia. Median SCV (finger-wrist) in farmers using Delsen (mancozeb, dithiocarbamate fungicide), who showed significant decrease of serum cholinesterase activities, were significantly lower compared with the controls. Sural SCV in farmers using Fastac (alpha-cypermethrin, pyrethroid insecticide) and median MCV (elbow-wrist) in farmers using Tamex (butralin, dinitroaniline herbicide) were significantly slowed compared with their respective controls. In Delsen (mancozeb, dithiocarbamate) users, the power of postural sway of 0-1 Hz was significantly larger than that in the controls both in the anterior-posterior direction with eyes open and in the right-left direction with eyes closed. The former type of sway was also significantly increased in Tamaron (methamidophos, organophosphorus insecticide) users. In conclusion, nerve conduction velocities and postural sway seem to be sensitive indicators of the effects of pesticides on the central and peripheral nervous system.     

Neurophysiological studies on workers exposed to lead.

Nerve conduction and somatosensory evoked potential studies were undertaken on 46 workers exposed to a combination of organic and inorganic lead. In addition electroencephalograms were carried out on 20 of the workers; the results were compared with those obtained for workers not exposed to lead. The workers exposed to lead had a mean blood lead concentration of 2.35 mumol/l (48.7 micrograms/100 ml), whereas the concentration for workers not exposed to lead was 0.76 mumol/l (15.8 micrograms/100 ml). The mean maximum motor conduction velocities of the median and the posterior tibial nerves were significantly lower in the workers exposed to lead than in the controls. Similarly, the distal latency for these two nerves was significantly prolonged for the workers exposed to lead. No significant differences for the two groups of workers were seen in the nerve conduction and distal latency measurements of the median (sensory) and the sural nerves. The EEG studies of the 20 workers exposed to lead showed no abnormalities. The somatosensory evoked potential of the median (sensory) and posterior tibial nerves were significantly prolonged when measured at the negative and positive deflections. The results suggest that, in addition to nerve conduction velocities, somatosensory evoked potential and distal latency are suitable measurements to detect subclinical neurological damage among workers exposed to lead. As these changes were seen at blood lead concentrations of 2.35 mumol/l (48.7 micrograms/100 ml) there may be a need for more stringent monitoring of workers exposed to lead.     

Neurophysiological studies on workers exposed to lead

Nerve conduction and somatosensory evoked potential studies were undertaken on 46 workers exposed to a combination of organic and inorganic lead. In addition electroencephalograms were carried out on 20 of the workers; the results were compared with those obtained for workers not exposed to lead. The workers exposed to lead had a mean blood lead concentration of 2.35 mumol/l (48.7 micrograms/100 ml), whereas the concentration for workers not exposed to lead was 0.76 mumol/l (15.8 micrograms/100 ml). The mean maximum motor conduction velocities of the median and the posterior tibial nerves were significantly lower in the workers exposed to lead than in the controls. Similarly, the distal latency for these two nerves was significantly prolonged for the workers exposed to lead. No significant differences for the two groups of workers were seen in the nerve conduction and distal latency measurements of the median (sensory) and the sural nerves. The EEG studies of the 20 workers exposed to lead showed no abnormalities. The somatosensory evoked potential of the median (sensory) and posterior tibial nerves were significantly prolonged when measured at the negative and positive deflections. The results suggest that, in addition to nerve conduction velocities, somatosensory evoked potential and distal latency are suitable measurements to detect subclinical neurological damage among workers exposed to lead. As these changes were seen at blood lead concentrations of 2.35 mumol/l (48.7 micrograms/100 ml) there may be a need for more stringent monitoring of workers exposed to lead.     

Subclinical lead neuropathy

It had been shown that subclinical impairment of the peripheral nerves may occur in neurologically symptom-free lead workers. In a cross-sectional study, 78 workers from two storage battery plants and one engineering shop were studied; their lead exposure had been monitored with regular blood lead measurements (PbB). The reference group comprised 34 unexposed manual workers. An exposure-effect relationship between occupational lead exposure and nerve functions emerged, as nerve conduction velocities decreased with increasing PbBs. The strongest correlations were found between PbB measures and sensory and motor conduction velocities of the median nerve. An exposure-response relationship also emerged as the proportion of subjects with abnormal nerves increased with increasing exposure levels. In a prospective study 24 workers were followed-up from the commencement of their lead work for one year and 16 for two years. The lead exposed showed a tendency of decreasing conduction velocities of arm nerves, but as a group they did not differ statistically significantly from the control group. When the lead exposed were divided into two groups using the median PbBs as the splitting point, the ones with PbBs over 30 micrograms/100 ml showed slowing of serveral nerve conduction velocities, while in the lower exposure the conduction velocities remained at the initial level. Again the clearest difference was noted in conduction velocities of the median nerve. Nerve conduction velocities, especially in the arm nerves slow down in lead exposure and this impairment is caused by really low lead exposure as noted in the prospective follow-up study, which can be regarded as intervention study.     

Relationships between lead absorption and peripheral nerve conduction velocities in lead workers.

The motor sensory, and mixed nerve conduction velocities of median and posterior tibial nerves were measured in 39 lead workers whose blood lead (PbB) concentrations ranged from 2 to 73 mug/100 g with anaverage of 29 mug/100 g. The PbB concentrations significantly correlated with the maximal motor nerve conduction velocities (MCV) and mixed nerve conduction velocities (MNCV) of the median nerve in the forearm and with the MCV of the posterior tibial nerve. Erythrocyte delta-aminolevulinic acid dehydratase (ALAD) activity correlated similarly with the MCV and MNCV of the median nerve in the forearm, and the 24-hour urinary lead excretion following the intravenous administration of CaEDTA (20 mg/kg) (lead mobilization test) correlated with the MNCV. But no parameter correlated with the sensory nerve conduction velocities. By multiple regression analysis, a combination of the three parameters of lead absorption was found to correlate significantly with the MCV and MNCV of the median nerve in the forearm. The MCVs of the median and posterior tibial nerves in lead workers were significantly delayed in the PbB range of 29-73 mug/100 g (mean 45), in the lead mobilization test range from 173 to 3,540 mug/day (mean 973), and the ALAD activity range from 4.4 to 19.4 u. (mean 14.0), respectively.     

Verification of effects on the nervous system of low level occupational exposure to CS2.

Neurotoxic effects associated with long term low level occupational exposure to CS2 were reinvestigated four years after the initial study in the same group of workers. The second study concerned 44 exposed and 31 matched control workers. For both studies a personal cumulative exposure Ec was calculated based on function specific exposure levels and the occupational histories, which were carefully re-established. The exposed workers' average Ec was 192 and 213 ppm-years (first and second study respectively). Where possible the values of both data sets were used in a final combined analysis. Effects were found on the motor nerve conduction velocity of the fast (-0.9 m/s) and slow (-1.0 m/s) fibres of the peroneal nerve, the sensory nerve conduction velocity in the hand and arm segment of the median (-2.1 m/s) and ulnar (-1.3 m/s) nerves, and in the sural nerve (-1.3 m/s). An increased refractory period was found in the sural nerve (+ 0.2 ms, + 11%), but not in the peroneal nerve. For the autonomic nervous system an effect was found on the heart frequency response to isometric muscle contraction (-4.7 beats/min, -26%) and maximal forced respiration (-3.2 beats/min, -16%). This study shows the importance of a detailed evaluation of past exposure data. The reinvestigation enabled a more precise estimation of the effects of CS2, which is particularly desirable at around threshold exposure.     

Peripheral nerve conduction velocities in chain-saw operators.

The motor, sensory and mixed nerve conduction velocities of median and posterior tibial nerves were measured in seventeen forest workers engaged in chain-saw operation for 2 to 16 yr (mean 12 yr). The conduction velocities were significantly diminished in the distal part of the upper limb. The sensory nerve conduction velocities (SCV) of the median nerve at the part of the palm were slow in 12 workers; longer residual latency, in 6; and the mixed nerve conduction velocities slowed at the part of the forearm, in 6. From the relationships of the nerve conduction velocities to white finger attacks and electromyograms, it was assumed that vibration directly affected the distal part of the sensory and motor nerve fibers in the upper limbs, and that the diminished SCV in the palm was one of the most sensitive indices of vibration effects.     

Electrophysiology and nerve biopsy in men exposed to lead

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.     

Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function

This study aimed to investigate whether occupational exposure to organophosphate (OP) pesticides caused neurophysiological abnormalities. Thirty farmers who regularly spray OP pesticides and 30 fishermen (controls), living close by but not involved in pesticide spraying, were evaluated during and between cultivation seasons. The farmers had higher erythrocyte acetylcholinesterase levels than the controls during (P = 0.06) and between cultivation seasons (P = 0.09). During the cultivation season, there was a significant reduction in erythrocyte acetylcholinesterase activity in both groups (P < 0.01). Significant differences between the farmers and controls were found in sensory conduction velocity (P = 0.04) and motor conduction velocity (P = 0.04) between cultivation seasons. Sensory conduction velocity was reduced significantly in farmers (P < 0.01) and in controls (P = 0.04) during the cultivation season. Effects of OP poisoning were seen both in farmers and in controls, who had no history of spray activities. Evidence of sensory dysfunction after acute exposure and sensory and motor impairment after long-term low-level exposure to OP was seen.     

Tocotrienol-Rich Vitamin E (Tocovid) Improved Nerve Conduction Velocity in Type 2 Diabetes Mellitus Patients in a Phase II Double-Blind,Randomized Controlled Clinical Trial

Diabetic peripheral neuropathy (DPN) is the most common microvascular complication of diabetes that affects approximately half of the diabetic population. Up to 53% of DPN patients experience neuropathic pain, which leads to a reduction in the quality of life and work productivity. Tocotrienols have been shown to possess antioxidant, anti-inflammatory, and neuroprotective properties in preclinical and clinical studies. This study aimed to investigate the effects of tocotrienol-rich vitamin E (Tocovid Suprabio^TM) on nerve conduction parameters and serum biomarkers among patients with type 2 diabetes mellitus (T2DM). A total of 88 patients were randomized to receive 200 mg of Tocovid twice daily, or a matching placebo for 12 months. Fasting blood samples were collected for measurements of HbA1c, renal profile, lipid profile, and biomarkers. A nerve conduction study (NCS) was performed on all patients at baseline and subsequently at 2, 6, 12 months. Patients were reassessed after 6 months of washout. After 12 months of supplementation, patients in the Tocovid group exhibited highly significant improvements in conduction velocity (CV) of both median and sural sensory nerves as compared to those in the placebo group. The between-intervention-group differences (treatment effects) in CV were 1.60 m/s (95% CI: 0.70, 2.40) for the median nerve and 2.10 m/s (95% CI: 1.50, 2.90) for the sural nerve. A significant difference in peak velocity (PV) was also observed in the sural nerve (2.10 m/s; 95% CI: 1.00, 3.20) after 12 months. Significant improvements in CV were only observed up to 6 months in the tibial motor nerve, 1.30 m/s (95% CI: 0.60, 2.20). There were no significant changes in serum biomarkers, transforming growth factor beta-1 (TGFβ-1), or vascular endothelial growth factor A (VEGF-A). After 6 months of washout, there were no significant differences from baseline between groups in nerve conduction parameters of all three nerves. Tocovid at 400 mg/day significantly improve tibial motor nerve CV up to 6 months, but median and sural sensory nerve CV in up to 12 months of supplementation. All improvements diminished after 6 months of washout.     

Association between chronic exposure to arsenic and slow nerve conduction velocity among adolescents in Taiwan

The association between chronic exposure to arsenic and peripheral neuropathy has been controversial in previous studies, which may be due to the influence of factors, such as age, gender, chronic diseases, occupational injuries, and arsenic exposure. To clarify the question of this association, a cross-sectional study was designed. In total, 130 junior high school students aged 12-14 years were included and examined for the motor and sensory nerve conduction velocity of peripheral nerves in their right-upper and lower limbs. Concentrations of arsenic in well-water and history of drinking well-water were retrieved from a baseline database created in 1991. After adjustment for gender and height, a significant odds ratio of 2.9 (95% confidence interval [CI] 1.1-7.5) was observed for the development of slow nerve conduction velocity of the sural sensory action potential (SAP) among the study subjects with a cumulative arsenic dosage of>100.0 mg. In addition, a borderline statistical significance with odds ratio of 7.8 (95% CI 1.001-69.5) for the development of slow nerve conduction velocity of sural SAP was also observed among the study subjects who drank well-water containing arsenic concentrations of >50.0 microg/L and with a cumulative arsenic dosage of >100.0 mg. The study found that chronic exposure to arsenic might induce peripheral neuropathy. It also found that the slowing of the nerve conduction velocity of sural SAP might be an early marker of chronic arsenic neuropathy.     

Rural work and pesticide poisoning

Pesticide use is intensive in Brazilian agriculture. Population-based studies on the characteristics of pesticide use and pesticide poisoning are scarce. This study describes the profile of occupational exposure and pesticide poisoning incidence. Farm characteristics and pesticide occupational exposure were evaluated using a cross-sectional design. Among 1,379 farmers/farm workers, annual incidence of pesticide poisoning was 2.2 episodes per 100 exposed. Based on Poisson regression, applying pesticide, reentering crop fields after spraying, and working with pesticides on more than one farm were the types of exposure that presented a positive correlation with pesticide poisoning. The results may be useful for planning activities aimed at reducing occupational pesticide poisoning among rural workers.     

Neuropathy and the automatic analysis of electromyographic signals from vibration exposed workers.

An automatic analysis of the electromyographic activity of the extensor digitorum communis, first dorsal interosseus and opponens pollicis muscles was performed, and both motor and sensory conduction velocities of the median and ulnar nerves were measured in the study of neuropathic changes that occur in traumatic vasospastic disease. Twenty-eight forest workers and 10 pneumatic-tool operators, all with a long occupational exposure to local vibration of the hands, were studied with these neurophysiological methods and general clinical and roentgenological examinations. Twenty male manual workers with a similar age distribution served as the comparison group. The most sensitive measures which separated the subjects with traumatic vasospastic disease from the nonexposed workers were the conduction velocity of the slower motor fibers of the ulnar nerve, the distal sensory conduction velocity and the motor distal latency of the median nerve. The duration and rise time of the averaged muscular potentials of intrinsic hand muscles correlated especially with those nerve conduction velocities which were the most sensitive in exhibiting neuropathic changes.     

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

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 mumol/l, 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 concluded that the effect of lead on the conduction velocity of the motor nerves has an initial reversible phase, dependent on the duration of exposure.     

A cross-sectional study of triallate exposure and neurological health among workers at a pesticide manufacturing and formulating facility

Aims: To evaluate the relation between an indicator of cumulative exposure to triallate and selected measures of neurological function, including nerve conduction, the prevalence of certain neurological deficits as determined by a medical examination, and vibration perception threshold testing in workers at a pesticide manufacturing plant.

Methods: Subjects were 50 workers with high estimated triallate exposure ("high triallate" group) and 50 workers with no or low triallate exposure ("no/low triallate" group). Industrial hygienists used existing work histories and personal knowledge of plant operations to develop a triallate score. In-person interviews elicited information on past medical history and on occupational and non-occupational exposures. A neurologist carried out nerve conduction tests of the sural and the peroneal nerves, a standardised neurological examination, and vibration sensation testing.

Results: Differences between the high and the no/low triallate groups were minimal for all but one of the six nerve conduction tests, for the prevalence of neurological abnormalities, and for vibration sensation perception. The high triallate group had lower mean sural nerve peak amplitude than the no/low triallate group (11.7 v 15.2 µV, p = 0.03). This difference was reduced when adjusted for other potential risk factors (12.5 v 14.5 µV, p = 0.25) and was not associated with cumulative triallate score. We also noted several associations between factors other than triallate and nerve conduction measures.

Conclusion: The results were consistent with the absence of an association between triallate and measures of neurological function.

     

Reversible nerve lesions after accidental polychlorinated biphenyl exposure

Several capacitors containing polychlorinated biphenyls (PCB) exploded in a cardboard plant. During the accident, and in the clearing work, several workers were in probable contact with PCB and/or its degradation products. Nausea, intense perspiration, and headache were acute symptoms, which cleared quickly. The 15 men with the greatest exposure were studied neurophysiologically twice, namely, two and six months after the explosion. Motor conduction velocities (MCV) of the right median, ulnar, and peroneal nerves; sensory conduction velocity (SCV) of the right sural nerve; and distal SCVs of the right median and ulnar nerves were measured with skin electrodes. Thirty male workers with a similar age distribution served as referents. Two months after the explosion all SCVs and distal SCVs were slower in the exposed men, and still six months after the explosion the distal SCV of the ulnar nerve and the SCV of the sural nerve were slightly slower among the exposed. However, clear improvement occurred in the distal SCVs during the follow-up. As in many toxic distal axonopathies, the distal SCVs were reversibly impaired after an accidental exposure to PCB fumes. PCB seem to exhibit neurotoxic properties in humans.     

Nerve conduction velocity studies of workers employed in the manufacture of phenoxy herbicides

Conduction velocities (NCV) of the median motor, median sensory, and sural nerves were measured in 56 workers employed in the manufacture of 2,4,5-trichlorophenoxy acetic acid (2,4,5-T) and 2,4-dichlorophenoxy acetic acid (2,4-D). Mean age was 35 years and mean duration of employment was 7 years. The control group consisted of 25 subjects without exposure to neurotoxic agents. When compared with controls, slowing was noted in the sural nerve (mean = 34.0 vs 40.1 m/sec, P > 0.02). All values were then adjusted for age and temperature and were transformed to Z values (mean = 0, standard deviation = 1), where-upon slowing was seen in the sural (?2.21 vs ?0.52, P < 0.0001) and median motor nerves (0.19 vs 0.91, P < 0.03). Duration of employment was significantly correlated with slowing of sural velocity (r = ?0.40, P < 0.004). Altogether, 46% of the study group had one or more slowed nerve conduction velocity, versus 5% of the control group P < 0.001).     

Assessment of exposure to arsenic among smelter workers: A five-year follow-up

In a group of 43 smelter workers exposed to inorganic arsenic dust for 13-45 years, nerve conduction velocities (NCVs) were significantly lower in two peripheral nerves as compared with matching referents. With multivariate data analysis, a significant negative correlation was found between cumulative absorption of arsenic and NCV in four examined nerves and the sural amplitude. Clinical symptoms of neuropathy and other symptoms related to arsenic exposure were moderate, though the difference between the groups was significant. The mean total absorption of arsenic was calculated to be less than 5 g, and the maximal absorption about 20 g. These data indicate that the adverse effect of arsenic on the peripheral nerves is dependent on long-term exposure rather than on short-term fluctuations in exposure levels. © 1994 Wiley-Liss, Inc.     

Combined electroneurographic and electromyographic studies in lead workers.

OBJECTIVES--To evaluate the effects of chronic exposure to lead on the peripheral nervous system in lead workers. METHODS--Nerve conduction velocity and electromyographic studies were performed on 31 lead workers of a battery recycling factory and 31 sex and age matched controls. 25 cases with mild distal extensor weakness of the upper limbs were classified as the lead neuropathy subgroup and the rest of the lead workers as the lead exposure subgroup. Blood lead concentrations and haematological and biochemical data were recorded. An index of cumulative exposure to lead was calculated by the summation of multiplying the average blood concentration of lead with the duration of exposure at various jobs. RESULTS--Compared with the control group, the distal motor latency of the median nerve was significantly prolonged in the lead neuropathy subgroup, but not in the exposure subgroup. Only six of 31 workers had nerve conduction abnormalities, whereas electromyographic evidence of denervation was found in 93.5% of the lead neuropathy subgroup and 83.5% in the lead exposure subgroup. The electromyographic abnormalities found were neurogenic polyphasic waves in all 29 workers with abnormal electromyographic findings (grade in seven cases and grade ++ in the rest). Spontaneous activity was only recorded in seven workers, with grade + in four and grade ++ in three. There was a positive linear correlation between the index of cumulative exposure to lead and the distal motor latencies of the tibial nerve as well as a negative correlation with conduction velocities of the sural nerve after multivariate analysis and control of potential confounding by age and sex. No correlation could be found between the electrophysiological values and a simple duration of exposure or concentration of blood lead. A non-parametric analysis showed that there was a trend of higher index of cumulative exposure to lead with more severe electromyographic changes. Electromyographic abnormality also occurred in workers with blood lead concentrations between 17.4 and 58 micrograms/dl. CONCLUSION--Electromyographic study in the distal extensors of the upper limbs may be used as a tool for biological monitoring of effect in lead workers.     

An electroneurographic assessment of subclinical lead neurotoxicity

Summary While heavy exposure to inorganic lead is capable of inducing symptomatic neuropathy in man, the subclinical neuropathy due to low levels of occupational lead exposure remains to be proved. The reported results of electroneurographic studies on lead workers, however, have been controversial. In this study, 40 lead smeltery workers and 50 non-exposed referents were investigated. The air concentrations of lead at worksites were 0.25 to 42.5 mg/m³. The geometric means of PbB, PbU and -ALAU in lead exposed group were 40.03 g/dl, 71 g/l and 4.68 mg/l respectively, which were significantly higher (P < 0.001) than those (7.01 g/dl, 6.0 g/l and 1.81 mg/l respectively) in the reference group. There were no clinical symptoms or signs of nerve damage in either group. Alcoholism and diabetes were excluded in both groups. Nerve conduction velocity was measured by a DISA 1500 electromyograph in both groups. Eleven electroneurographic parameters, including motor nerve conduction velocity (MCV) and distal latency (DML) of median, ulnar and peroneal nerves as well as sensory nerve conduction velocity (SCV) and distal latency (DSL) of median, ulnar and sural nerves, showed statistically significant differences between the two groups. However, the results of electroneurographic measurements of each individual in the lead-exposed group were all within the normal range. There was no correlation between the bloodlead levels and the neurophysiological measurements except for the median MCV. No correlation was seen between the median MCV and the exposure duration. A reduction in MCVs of median and ulnar nerves and sural SCV was unexpectedly seen in eight lead workers after chelation therapy with CaEDTA, although their mean PbB decreased from 42.08 to 27.92 g/dl. No consistent findings in nerve conduction were found at these exposure levels.