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 on the peripheral nervous system of tunnel workers exposed to acrylamide and N-methylolacrylamide

OBJECTIVES: This study evaluates the possible toxic effects on the peripheral nervous system of tunnel workers exposed to acrylamide and N-methylolacrylamide during grouting work. METHODS: Symptoms and nerve conduction velocities (NCV) were recorded for 24 tunnel workers 4 and 16 months after the cessation of exposure during grouting operations. Fifty tunnel workers not involved in grouting operations served as referents. Exposure was assessed by questionnaires, qualitative exposure indices, and measurements of hemoglobin adducts after the cessation of exposure. RESULTS:The exposed workers reported a higher prevalence of symptoms during grouting work than they did in an examination 16 months later. A statistically significant reduction in the mean sensory NCV of the ulnar nerve was observed 4 months postexposure when compared with the values of the reference group (52.3 versus 58.9 m/s, P = 0.001), and the mean ulnar distal delay was prolonged (3.1 versus 2.5 ms, P = 0.001). Both measures were significantly improved when measured 1 year later. Exposure-related improvements were observed from 4 to 16 months postexposure for both the median (motor and sensory NCV and F-response) and ulnar (sensory NCV, F-response) nerves. A significant reversible reduction in the mean sensory amplitude of the median nerve was also observed, while the mean sensory amplitude of the sural nerve was significantly reduced after 16 months. CONCLUSIONS: The results indicate demyelinating and axonal changes in peripheral nerves of tunnel workers in relation to exposure to N-methylolacrylamide and acrylamide during grouting operations. The changes were slight, mostly subclinical, and most of the effects were reversible, with normalization after 1 year.     

Occupational exposure to pesticides and nerve conduction studies among Korean farmers

This study aimed to determine whether occupational exposure to pesticides was associated with decreased nerve conduction studies among farmers. On 2 separate occasions, the authors performed a cross-sectional study of a group of 31 male farmers who periodically applied pesticides. The study included questionnaire interviews and nerve conduction studies on the median, ulnar, posterior tibial, peroneal, and sural nerves. Although all mean values remained within laboratory normal limits, significant differences between the first and second tests were found in sensory conduction velocities on the median and sural nerves, and motor conduction velocities on the posterior tibial nerve. Lifetime days of pesticide application was negatively associated with nerve conduction velocities at most nerves after adjusting for potential confounders. These findings may reflect a link between occupational pesticide exposure and peripheral neurophysiologic abnormality that deserves further evaluation.     

Electroneurographic findings in workers exposed to mercury]

25 mercury-exposed workers as well as 27 age-matched controls were investigated in an electroneurographic study. The population of mercury-exposed workers was found to have --an increased latency of distal motor action potential at both median and peroneal nerves --an increased latency of distal sensory action potential at median nerve --a decrease of amplitudes of evoked muscle potentials at both median and peroneal nerves --a reduced motor nerve conduction velocity at both examined nerves --a reduced antidromic sensory nerve conduction velocity at median nerve. To detect early changes in nerval function we recommend regularly electroneurographic examinations of mercury-exposed people.     

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).     

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.     

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.     

Peripheral neurotoxicity in workers exposed to inorganic mercury compounds

Nerve conduction velocity (NCV) of the median motor, median sensory, and sural nerves was assessed in 16 workers chronically exposed to various inorganic mercury compounds. Exposed workers were compared with an unexposed control group using t test analyses. Slowing of the median motor nerve NCV was found, which was correlated with both increased levels of mercury in blood and urine, and with increased number of neurologic symptoms. Sensitive evaluation of neural function was found to be practical and informative for investigating mercury toxicity. Such evaluation can help determine safe mercury levels at the workplace.     

Relation between exposure related indices and neurological and neurophysiological effects in workers previously exposed to mercury vapour.

A cross sectional study of aspects of their neurology was carried out on 77 chloralkali workers previously exposed to mercury (Hg) vapour and compared with 53 age matched referents. The chloralkali workers had been exposed for an average of 7.9 years at a concentration of 59 micrograms Hg/m3 in the working atmosphere. The individual mean urinary concentration of Hg for each year of exposure was 531 nmol Hg/1. On average the exposure had ceased 12.3 years before the examinations. Both the median sensory nerve conduction velocity and the amplitude of the sural nerve were associated with measures of cumulative exposure to Hg. An association was also found between years since first exposure to Hg and aspects of the visual evoked response. Previously exposed subjects with postural tremor or impaired coordination also had alterations in visual evoked response. These results may indicate an effect of previous exposure to mercury vapour on the nervous system, possibly in the visual pathway, cerebellum, and the peripheral sensory nerves.     

Effect of perinatal food deficiencies on the compound action potential evoked in sensory nerves of developing rats

The aim of this study was to analyze the possible alterations produced by inadequate perinatal food intake, in quantity (undernutrition) or quality (malnutrition), on the generation and propagation of the compound action potential (CAP) evoked in sensory sural nerves, during the postnatal development of the rat. Low intensity stimulation (2-3 times the threshold of the most excitable nerve fibers; xT) of the sural nerve evoked an early potential (CAP-A component) which is due to activation of low-threshold, fast-conducting myelinated group A afferent fibers. Meanwhile, at higher stimulus intensity (20-30T) it produced a second, long-lasting potential (CAP-C component) probably due to activation of high-threshold, slow-conducting group Adelta or C afferent fibers. Compared to control nerves, the CAP-A component, but not the CAP-C component of undernourished and malnourished nerves showed significant changes in amplitude, area, electrical threshold and conduction velocity (except absolute refractory period) at several postnatal ages. Our results may suggest that a relative large number of myelinated group A afferent fibers in the sural nerve of undernourished and malnourished animals suffer severe alterations on their electrophysiological properties of generation and propagation of the action potential during the postnatal development of the rat.     

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.     

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.     

Normal nerve conduction velocity and vibrotactile perception thresholds in computer users

OBJECTIVES: A literature report described significantly raised vibration threshold within the territory of the median nerve in a group of office workers and concluded that the results indicated a change in the function of large sensory fibres. The aim of the present cross-sectional study was to compare vibrotactile perception thresholds and nerve conduction measurements in the upper extremity between female computer users (secretaries) and female non-users (nurses). METHODS: Eighty-two secretaries, aged 25-65 (median 44) years and 35 nurses, aged 24-57 (median 46) years went through nerve conduction measurements on the dominant hand and also a vibration threshold test with readings over the hand at five sites which tested cutaneous innervation of the median, ulnar, and radial nerves. RESULTS: There was no significant difference in any parameter of the nerve conduction testing and there was no significant difference in any parameter of the vibration threshold test between secretaries and nurses. The numerical differences between groups were small and in both directions and thus do not indicate a power problem. CONCLUSIONS: We saw no signs of early neural deficits of large sensory fibres in subjects who intensively use computer keyboard equipment.     

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.     

Nerve function in workers with long term exposure to trichloroethene.

Certain functions of the nervous system were examined in 31 printing workers (mean age 44) exposed to trichloroethene (mean duration 16 years) and 28 controls (mean age 45). In the sural nerve the conduction velocity (SNCV), response amplitude, and refractory period (SRP) were measured. The latencies of the masseter and the blink reflex were determined to test the trigeminal nerve. In the peroneal nerve the conduction velocity of fast and slow nerve fibres, the response amplitude, and the refractory period were determined. As a measure of autonomic nerve function the response of the heart rate was determined to isometric muscle contraction and deep breathing. Individual cumulative exposure was calculated on the basis of exposure levels in the past. The mean cumulative exposure of the exposed workers was 704 ppm x years. For the assessment of the exposure effect relation a multiple linear regression model was used. A slight reduction (-1.1 m/s) in the SNCV was found and a prolongation (0.4 ms) of the SRP (mean of the controls 1.95 ms). The latency of the masseter reflex (mean 10.4 ms) had increased (0.4 ms). With respect to the blink reflex no prolongation was found. No impairment was found in the functions of motor and autonomic nerves. This study shows that the refractory period may be a sensitive indicator of preclinical toxic neuropathies. Long term exposure to trichloroethene at threshold limit values (about 35 ppm) may slightly affect the trigeminal and sural nerves.     

Nerve function in workers with long term exposure to trichloroethene

Certain functions of the nervous system were examined in 31 printing workers (mean age 44) exposed to trichloroethene (mean duration 16 years) and 28 controls (mean age 45). In the sural nerve the conduction velocity (SNCV), response amplitude, and refractory period (SRP) were measured. The latencies of the masseter and the blink reflex were determined to test the trigeminal nerve. In the peroneal nerve the conduction velocity of fast and slow nerve fibres, the response amplitude, and the refractory period were determined. As a measure of autonomic nerve function the response of the heart rate was determined to isometric muscle contraction and deep breathing. Individual cumulative exposure was calculated on the basis of exposure levels in the past. The mean cumulative exposure of the exposed workers was 704 ppm x years. For the assessment of the exposure effect relation a multiple linear regression model was used. A slight reduction (-1.1 m/s) in the SNCV was found and a prolongation (0.4 ms) of the SRP (mean of the controls 1.95 ms). The latency of the masseter reflex (mean 10.4 ms) had increased (0.4 ms). With respect to the blink reflex no prolongation was found. No impairment was found in the functions of motor and autonomic nerves. This study shows that the refractory period may be a sensitive indicator of preclinical toxic neuropathies. Long term exposure to trichloroethene at threshold limit values (about 35 ppm) may slightly affect the trigeminal and sural nerves.     

Effect of Perinatal Food Deficiencies on the Compound Action Potential Evoked in Sensory Nerves of Developing Rats

The aim of this study was to analyze the possible alterations produced by inadequate perinatal food intake, in quantity (undernutrition) or quality (malnutrition), on the generation and propagation of the compound action potential (CAP) evoked in sensory sural nerves, during the postnatal development of the rat. Low intensity stimulation (2–3 times the threshold of the most excitable nerve fibers; X T) of the sural nerve evoked an early potential (CAP-A component) which is due to activation of low-threshold, fast-conducting myelinated group A afferent fibers. Meanwhile, at higher stimulus intensity (20–30T) it produced a second, long-lasting potential (CAP-C component) probably due to activation of high-threshold, slow-conducting group Aδ or C afferent fibers. Compared to control nerves, the CAP-A component, but not the CAP-C component of undernourished and malnourished nerves showed significant changes in amplitude, area, electrical threshold and conduction velocity (except absolute refractory period) at several postnatal ages. Our results may suggest that a relative large number of myelinated group A afferent fibers in the sural nerve of undernourished and malnourished animals suffer severe alterations on their electrophysiological properties of generation and propagation of the action potential during the postnatal development of the rat.     

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.     

苯对接触工人外周神经传导速度的影响

[目的 ]探讨苯对周围神经系统的影响。 [方法 ]对苯接触观察对象 13人、苯中毒者 14人为接触组 ,另选无毒物接触史的工人 48人为对照组 ,应用神经肌电图检测方法进行运动和感觉神经传导速度测定。 [结果 ]接触组尺神经及下肢腓浅神经感觉传导速度显著慢于对照组 (P <0 .0 5 ) ,其余所检神经传导速度与对照组相比差异无显著性 (P >0 .0 5 )。接触组下肢腓浅神经感觉传导速度异常率显著高于对照组。正中神经远端潜伏期较对照组明显延长 (P <0 .0 5 )。[结论 ]苯对周围神经存在一定程度的影响 ,感觉神经传导速度对于诊断周围神经病的价值优于运动神经传导速度