Occupational lead neurotoxicity: improvement in behavioural effects after reduction of exposure.

To evaluate critical exposure levels and the reversibility of lead neurotoxicity a group of lead exposed foundry workers and an unexposed reference population were followed up for three years. During this period, tests designed to monitor neurobehavioural function and lead dose were administered. Evaluations of 160 workers during the first year showed dose dependent decrements in mood, visual/motor performance, memory, and verbal concept formation. Subsequently, an improvement in the hygienic conditions at the plant resulted in striking reductions in blood lead concentrations over the following two years. Attendant improvement in indices of tension (20% reduction), anger (18%), depression (26%), fatigue (27%), and confusion (13%) was observed. Performance on neurobehavioural testing generally correlated best with integrated dose estimates derived from blood lead concentrations measured periodically over the study period; zinc protoporphyrin levels were less well correlated with function. This investigation confirms the importance of compliance with workplace standards designed to lower exposures to ensure that individual blood lead concentrations remain below 50 micrograms/dl.     

Occupational lead neurotoxicity: improvement in behavioural effects after reduction of exposure

To evaluate critical exposure levels and the reversibility of lead neurotoxicity a group of lead exposed foundry workers and an unexposed reference population were followed up for three years. During this period, tests designed to monitor neurobehavioural function and lead dose were administered. Evaluations of 160 workers during the first year showed dose dependent decrements in mood, visual/motor performance, memory, and verbal concept formation. Subsequently, an improvement in the hygienic conditions at the plant resulted in striking reductions in blood lead concentrations over the following two years. Attendant improvement in indices of tension (20% reduction), anger (18%), depression (26%), fatigue (27%), and confusion (13%) was observed. Performance on neurobehavioural testing generally correlated best with integrated dose estimates derived from blood lead concentrations measured periodically over the study period; zinc protoporphyrin levels were less well correlated with function. This investigation confirms the importance of compliance with workplace standards designed to lower exposures to ensure that individual blood lead concentrations remain below 50 micrograms/dl.     

Neurobehavioural effects of occupational exposure to lead.

A set of neurobehavioural tests selected on the basis of information processing theory was used to study the effect of low level occupational lead exposure on 59 lead workers compared with a matched control group of the same number. Only one of the lead exposed group had a blood lead concentration above the current threshold limit value of 3.81 mumol/l at the time of testing (mean 2.36 mumol/l, range 1.19-3.92 mumol/l) and none had been detected above that level in the previous three years. Nevertheless, most neurobehavioural functions tested showed some impairment in the lead workers. Visual sensory function was affected and, perhaps as a consequence, sustained attention and psychomotor tasks were performed more slowly by the lead exposed group. Cognitive functions were also impaired, with sensory store memory, short term memory, and learning abilities all showing deficits in lead workers. Such cognitive deficits may also be partly due to initial degradation of the visual input. Long term memory performance compared equally with control levels possibly because of development of a compensatory strategy such as rehearsal by the lead exposed subjects. Multiple linear regression analysis relating to lead workers test performance and their lead exposure showed that performance on the sensory store memory test alone was significantly related to exposure. This was probably due to the homogeneity of the lead exposed group with regard to blood lead concentrations and the use of blood lead as a measure of chronic lead exposure.     

Neurobehavioural effects of occupational exposure to lead

A set of neurobehavioural tests selected on the basis of information processing theory was used to study the effect of low level occupational lead exposure on 59 lead workers compared with a matched control group of the same number. Only one of the lead exposed group had a blood lead concentration above the current threshold limit value of 3.81 mumol/l at the time of testing (mean 2.36 mumol/l, range 1.19-3.92 mumol/l) and none had been detected above that level in the previous three years. Nevertheless, most neurobehavioural functions tested showed some impairment in the lead workers. Visual sensory function was affected and, perhaps as a consequence, sustained attention and psychomotor tasks were performed more slowly by the lead exposed group. Cognitive functions were also impaired, with sensory store memory, short term memory, and learning abilities all showing deficits in lead workers. Such cognitive deficits may also be partly due to initial degradation of the visual input. Long term memory performance compared equally with control levels possibly because of development of a compensatory strategy such as rehearsal by the lead exposed subjects. Multiple linear regression analysis relating to lead workers test performance and their lead exposure showed that performance on the sensory store memory test alone was significantly related to exposure. This was probably due to the homogeneity of the lead exposed group with regard to blood lead concentrations and the use of blood lead as a measure of chronic lead exposure.     

Occupational lead neurotoxicity: a behavioural and electrophysiological evaluation. Study design and year one results.

To evaluate the effects of chronic lead exposure on the nervous system in adults, a set of neurobehavioural and electrophysiological tests was administered to 99 lead exposed foundry employees and 61 unexposed workers. Current and past blood lead concentrations were used to estimate the degree of lead absorption; all previous blood lead concentrations had been less than or equal to 90 micrograms/100 ml. Characteristic signs (such as wrist extensor weakness) or symptoms (such as colic) of lead poisoning were not seen. Sensory conduction in the sural nerve was not affected. By contrast, various neurobehavioural functions deteriorated with increasing lead burden. Workers with blood lead concentrations between 40 and 60 micrograms/100 ml showed impaired performance on tests of verbal concept formation, visual/motor performance, memory, and mood. Thus impairment in central nervous system function in lead exposed adults occurred in the absence of peripheral nervous system derangement and increased in severity with increasing lead dose.     

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.     

Evaluation of delta-aminolaevulinic acid in blood of workers exposed to lead.

Exposure-effect and exposure-response relation between exposure to lead and delta-aminolaevulinic acid concentration in blood (ALA-B) were examined in 238 male workers exposed to lead. Concentrations of ALA-B ranged from 26 to 352 micrograms/l and lead concentrations in blood (Pb-B) from 7.1 to 86.0 micrograms/dl. Concentrations of ALA-B correlated closely with concentrations of Pb-B (r = 0.74), and increased ALA-B concentration occurred at Pb-B concentrations of around 30 micrograms/dl. Exposure-response curves indicated that the 50 percentile response doses were roughly 30, 40, and 50 micrograms/dl Pb-B when cut off points of ALA-B were set at 50, 60, and 70 micrograms/l respectively. The sensitivity and specificity of measurements of ALA-B concentrations for health screening were sufficiently high when the health based exposure limits of lead were set at 30-50 micrograms/dl. Moreover, a pronounced increase in ALA-B concentrations occurred when the inhibition rate of erythrocyte ALA dehydratase exceeded 85%. These findings suggest that ALA-B is a useful indicator for assessing the early effects of exposure to lead on haem biosynthesis.     

Body burdens of lead in hypertensive nephropathy

Chronic lead exposure resulting in blood lead concentrations that exceed 1.93 mumol/l (40 micrograms/dl) or chelatable urinary lead excretion greater than 3.14 mumol (650 micrograms) per 72 h has been associated with renal disease. A previous study had found greater chelatable urine lead excretion in subjects with hypertension and renal failure than in controls with renal failure due to other causes, although mean blood lead concentrations averaged 0.92 mumol/l (19 micrograms/dl). To determine if chelatable urinary lead, blood lead, or the hematologic effect of lead (zinc protoporphyrin) were greater in hypertensive nephropathy (when hypertension precedes elevation of serum creatinine) than in other forms of mild renal failure, we compared 40 study subjects with hypertensive nephropathy to 24 controls having a similar degree of renal dysfunction due to causes other than hypertension. Lead burdens were similar in both the study and control groups as assessed by 72-h chelatable urinary lead excretion after intramuscular injection of calcium disodium EDTA (0.74 +/- 0.63 vs. 0.61 +/- 0.40 mumol per 72 h, respectively), and by blood lead (0.35 +/- 0.23 vs. 0.35 +/- 0.20 mumol/l). We conclude that subjects from a general population with hypertensive nephropathy do not have greater body burdens of lead than renal failure controls.     

Male endocrine functions in workers with moderate exposure to lead.

Evidence for the effect of occupational exposure to lead on the male endocrine system is conflicting. This study evaluated the primary (testicular) and secondary (hypothalamo pituitary testicular) effects of exposure to lead in 122 current lead workers and 49 non-exposed workers. The mean current blood lead concentration was 35.2 (range 9.6-77.4) micrograms/dl in the exposed workers, and 8.3 (range 2.6-14.8) micrograms/dl in the non-exposed workers. Concentrations of plasma luteinising hormone (LH) and follicle stimulating hormone (FSH) were both significantly higher in the exposed workers, but testosterone (T) was not significantly different between the two groups. In older exposed workers, however (greater than or equal to 40 years), plasma T concentrations were significantly lower, but LH and FSH concentrations were not significantly different. Compared with non-exposed workers, those exposed for less than 10 years had significantly raised LH and FSH and normal T concentrations whereas those exposed for 10 or more years had significantly lower T, and normal LH and FSH concentrations. The concentrations of LH and FSH showed a moderate increase in relation to blood lead concentrations in the range of 10 micrograms/dl to 40 micrograms/dl and thereafter reached a plateau or declined. No apparent trend for plasma T concentrations occurred. No significant difference in prolactin (PRL) concentration was noted. It is concluded that moderate exposure to lead was associated in dose related fashion with small but measurable changes in male endocrine functions that reflected both primary and secondary effects of lead on the testes and the hypothalamo pituitary testicular axis.     

锰接触－行为功能关系的研究

选择４４名接触不同空气中锰浓度的干电池制造工和电焊工，进行了成套的神经行为功能测验。结果表明，接触组神经系统症状得分高于对照组，接触组语言、核心行为功能与指叩、积木图案、视觉再生、数字顺序和情感状态得分均低于对照组，其中语言和核心行为功能总得分与尿锰呈明显负相关。提示职业性长期锰接触后可能对神经行为功能产生损害，其损害程度与锰接触存在明显的接触水平－反应关系。     

Male endocrine functions in workers with moderate exposure to lead

Evidence for the effect of occupational exposure to lead on the male endocrine system is conflicting. This study evaluated the primary (testicular) and secondary (hypothalamo pituitary testicular) effects of exposure to lead in 122 current lead workers and 49 non-exposed workers. The mean current blood lead concentration was 35.2 (range 9.6-77.4) micrograms/dl in the exposed workers, and 8.3 (range 2.6-14.8) micrograms/dl in the non-exposed workers. Concentrations of plasma luteinising hormone (LH) and follicle stimulating hormone (FSH) were both significantly higher in the exposed workers, but testosterone (T) was not significantly different between the two groups. In older exposed workers, however (greater than or equal to 40 years), plasma T concentrations were significantly lower, but LH and FSH concentrations were not significantly different. Compared with non-exposed workers, those exposed for less than 10 years had significantly raised LH and FSH and normal T concentrations whereas those exposed for 10 or more years had significantly lower T, and normal LH and FSH concentrations. The concentrations of LH and FSH showed a moderate increase in relation to blood lead concentrations in the range of 10 micrograms/dl to 40 micrograms/dl and thereafter reached a plateau or declined. No apparent trend for plasma T concentrations occurred. No significant difference in prolactin (PRL) concentration was noted. It is concluded that moderate exposure to lead was associated in dose related fashion with small but measurable changes in male endocrine functions that reflected both primary and secondary effects of lead on the testes and the hypothalamo pituitary testicular axis.     

Exposure to neurotoxic metals among workers in Singapore: an overview

The extent of occupational exposure to inorganic lead, manganese,arsenic and inorganic mercury in Singapore was determined fromthe results of Statutory Medical Examinations and environmentalmonitoring carried out by the Department of Industrial Healthin 1989. There were 786 workers exposed to lead. Of these, 7.8per cent had blood levels greater than 40µg/dl. Therewere 67 workers exposed to mercury, 11.9 per cent of whom hadurinary mercury levels greater than 50µg/l. There were101 and 144 workers exposed to arsenic and manganese respectively.None of the biological samples exceeded the health-based limits.A review of local studies showed that some of the exposed workershad neurophysiological and neurobehavioural changes.     

Occupational lead poisoning in the United States: clinical and biochemical findings related to blood lead levels

Dose-response relationships between blood lead levels and toxic effects have been evaluated in 160 lead workers in two smelters and a chemicals plant. Blood lead levels ranged from 0.77 to 13.51 mumol/litre (16-280 microgram/dl). Clinical evidence of toxic exposure was found in 70 workers (44%), including colic in 33, wrist or ankle extensor muscle weakness in 12, anaemia (Hgb less than 8.69 mumol/litre (Hb/4) or 14.0 gm/dl) in 27, elevated blood urea nitrogen (greater than or equal to 7.14 mmol/litre or 20 mg/dl) in 28, and possible encephalopathy in two. No toxicity was detected at blood lead levels below 1.93 mumol/litre (40 microgram/dl). However, 13% of workers with blood lead levels of 1.93 to 3.81 mumol/litre (40-79 microgram/dl) had extensor muscle weakness or gastrointestinal symptoms. Anaemia was found in 5% of workers with lead levels of 1.93-2.85 mumol/litre (40-59 microgram/dl), in 14% with levels of 2.90 to 3.81 mumol/litre (60-79 microgram/dl), and in 36% with levels greater than or equal to 3.86 mumol/litre (80 microgram/dl). Elevated blood urea nitrogen occurred in long-term lead workers. All but three workers with increased blood urea nitrogen had at least four years occupational lead exposure, and nine had received oral chelation; eight of this group had reduced creatinine clearance, and eight had decreased renal concentrating ability. These data support the establishment of a permissible biological limit for blood lead at a level between 1.93 and 2.90 mumol/litre (40-60 microgram/dl).     

Occupational lead poisoning in the United States: clinical and biochemical findings related to blood lead levels.

Dose-response relationships between blood lead levels and toxic effects have been evaluated in 160 lead workers in two smelters and a chemicals plant. Blood lead levels ranged from 0.77 to 13.51 mumol/litre (16-280 microgram/dl). Clinical evidence of toxic exposure was found in 70 workers (44%), including colic in 33, wrist or ankle extensor muscle weakness in 12, anaemia (Hgb less than 8.69 mumol/litre (Hb/4) or 14.0 gm/dl) in 27, elevated blood urea nitrogen (greater than or equal to 7.14 mmol/litre or 20 mg/dl) in 28, and possible encephalopathy in two. No toxicity was detected at blood lead levels below 1.93 mumol/litre (40 microgram/dl). However, 13% of workers with blood lead levels of 1.93 to 3.81 mumol/litre (40-79 microgram/dl) had extensor muscle weakness or gastrointestinal symptoms. Anaemia was found in 5% of workers with lead levels of 1.93-2.85 mumol/litre (40-59 microgram/dl), in 14% with levels of 2.90 to 3.81 mumol/litre (60-79 microgram/dl), and in 36% with levels greater than or equal to 3.86 mumol/litre (80 microgram/dl). Elevated blood urea nitrogen occurred in long-term lead workers. All but three workers with increased blood urea nitrogen had at least four years occupational lead exposure, and nine had received oral chelation; eight of this group had reduced creatinine clearance, and eight had decreased renal concentrating ability. These data support the establishment of a permissible biological limit for blood lead at a level between 1.93 and 2.90 mumol/litre (40-60 microgram/dl).     

Occupational lead exposure of storage battery workers in Korea.

Two hundred and thirty-four lead workers employed in a storage battery factory in Korea were examined for lead in blood (PbB) and urine (PbU). delta-aminolaevulinic acid in urine (ALAU), coproporphyrin in urine (CPU), and haemoglobin. The dose-response relationship between PbB and ALAU suggested that a PbB below 50-60 micrograms/dl is a proper practical limit of biological monitoring for lead workers. The inter-relationship between PbB and ALAU or PbU was better explained by a segmental straight function than by a curvilinear function. Inclusion of data from workers whose PbB was below 30-40 micrograms/dl, if they comprise a relatively large proportion of the whole, seems to have a role as a dummy effect on the overall regression function causing the curvilinear trend. At a given blood lead concentration, the ALAU of lead workers increased with an increase in the duration of exposure. This could be explained by the chronic effect of lead on haem precursors. Semi-quantitative measurement of CPU still played an important part in the screening of lead workers due to its simplicity, showing high sensitivity (97.8%) in detecting lead workers with PbB of 60 micrograms/dl or over.     

Erythrocyte deformability in workers exposed to lead.

Erythrocyte deformability and other hematological indicators were determined in 17 male workers exposed to lead at a secondary lead refinery and 13 controls. Blood lead, urine lead, urine coproporphyrin, delta-aminolevulinic acid and erythrocyte zinc protoporphyrin were determined to evaluate the degree of lead exposure in the lead workers above. For the measurement of erythrocyte deformability, the microfilter method was used. The results were summarized as follows: 1. The mean values of blood lead, urine lead, urine coproporphyrin, urine delta-aminolevulinic acid and erythrocyte zinc protoporphyrin levels in lead workers were 53.5 micrograms/100g, 141.4 micrograms/l, 115.9 micrograms/l, 12.0 mg/l and 68.9 micrograms/dl respectively, suggesting a moderate influence of lead exposure. 2. The mean values of erythrocyte count, hematocrit and hemoglobin were significantly lower in lead workers than those in controls. No significant differences were found in the mean values of mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration and corpuscular natrium and potassium between lead workers and controls. 3. Erythrocyte deformability was significantly reduced in lead workers compared with controls.     

Clinical and neurobehavioural study of the acute and chronic neurotoxicity of styrene

A cross sectional field study of workers exposed to styrene was performed to evaluate possible acute and chronic neurotoxic effects. A total of 36 workers of four companies handling polyester resin materials for one to 16 years (median: 7 years) and two control groups were each examined on a Monday. The control group 1 (formed to compare acute effects) consisted of 20 men from two companies with no exposure to neurotoxic chemicals. To compare chronic effects, a second control group was formed by "one to one matching" with respect to age, socioeconomic status, and pre-exposure intelligence level. Ambient air monitoring using active sampling (short time) and passive samplers (long time) showed styrene in air concentrations as follows: range 3-251 ppm (median: 18 ppm) and concentrations 140-600 ppm during lamination of the inside of boats. For biological monitoring the results were as follows (postshift samples: range/median): styrene in blood: 5-482 micrograms/dl (39 micrograms/dl), mandelic acid urine: 0.01-3.64 g/l (0.21 g/l), and phenylglyoxylic acid urine: 0.01-0.87 g/l (0.19 g/l). The clinical examination found no signs or symptoms of peripheral neuropathy or encephalopathy. The principal work related health complaints were acute, reversible irritation of the eyes that occurred after exposure to styrene concentrations of 200 ppm or more. The neurobehavioural tests showed no significant differences in acute effects (p greater than 0.05) between the two groups or between preshift and postshift testing. Nor were there any significant differences in the relevant neurobehavioural variables between the styrene workers and the controls. It is concluded that occupational exposure to styrene concentrations in air up to 100 ppm causes no adverse acute or chronic effects on the central nervous system.     

血铅与红细胞游离原卟啉及锌原卟啉的剂量—效应关系

Studies on dose-effect relationships between blood lead (PbB) and free erythrocyte protoporphyrin (FEP) or zinc protoporphyrin (ZPP) in 583 workers (male 326, female 257) was conducted. Good dose-effect relationships and S-shaped curves between PbB and logFEP, logZPP or log (ZPP/Hb) were established. Sectioned linear regression showed that linear correlation was obtained while PbB between 0.48 (10 micrograms/dl) and 3.36 mumol/L (70 micrograms/dl) (male) or 0.48 (10 micrograms/dl) and 2.88 mumol/L (60 micrograms/dl) (female). However, while PbB below 0.48 mumol/L (10 micrograms/dl), there was no linear correlation. The increasing of FEP, ZPP slowed down remarkably as PbB were beyond 3.36 mumol/L (70 micrograms/dl) (male) or 2.88 mumol/L (60 micrograms/dl) (female). Therefore, the degree of lead poisoning can't be classified by the values of FEP, ZPP among plumbism.     

An investigation of the acute behavioural effects of styrene on factory workers.

A group of men exposed to styrene in a factory building glass-fibre boats performed a series of behavioural tests at the beginning and end of their shift, and the results were compared with those of a referent group from the same factory. Changes in mood were noted in both groups of workers but were greater in the exposed men; moreover, the change in mood was correlated with blood styrene concentration. In the styrene workers the morning reaction time was slower than that for the referents. During the day the reaction time of the men with low blood styrene concentration (less than or equal to 5.4 mumol/l) speeded up and in the afternoon was similar to that of the referents; the reaction time for the men with high blood styrene concentration (greater than or equal to 5.5 mumol/l) was unchanged. Data taken from a questionnaire indicated that the men exposed were much more likely than was the referent group to report feeling unduly tired. They also reported feeling more tired on Friday night than Monday night, suggesting that the styrene might have a cumulative effect through the week.