Subjective symptoms and psychological performance of chlorine-alkali workers

Subjective symptoms and psychological performances on a computer-administered test battery were studied among a group of 60 chlorine-alkali workers and their matched referents. The exposure time of the group exposed to inorganic mercury vapor had been about 14 years, and the estimated long-term average exposure had been about 25 micrograms/m3 of air. The exposed workers had an actual mercury concentration of 51.9 (SD 25.0, range 15-150) nmol/l in blood and 84.1 (SD 56.6, range 15-260) nmol/l in urine. Neither perceptual motor nor memory nor learning abilities of the mercury-exposed workers showed any disturbances in a comparison with the referents. However, the exposed group reported statistically significantly more memory disturbances than the referents. Strain caused by three-shift work was a possible cofactor for other increased subjective symptoms, namely, for sleep disorders, fatigue, and confusion.     

Surveillance of workers exposed to mercury vapour:validation of a previously proposed biological threshold limit value for mercury concentration in urine

A cross-sectional epidemiological study was carried out among subjects exposed to mercury (Hg) vapour, ie, a group of 131 male workers (mean age: 30.9 yr; average duration of exposure, 4.8 yr) and a group of 54 female workers (mean age, 29.9 yr; average duration of exposure 7 yr). The results were compared with those obtained in well-matched control groups comprising 114 and 48 male and female workers, respectively. The intensity of current Hg vapour exposure was rather moderate as reflected by the levels of mercury in urine (HgU) (mean and 95th percentile: males 52 and 147 micrograms/g creatinine; females 37 and 63 micrograms/g creatinine) and of mercury in blood (mean and 95th percentile: males 1.4 and 3.7 micrograms/dl; females 0.9 and 1.4 microgram/dl). Several symptoms mainly related to the central nervous system (memory disturbances, depressive feelings, fatigue, irritability) were more prevalent in the Hg-exposed subjects. They were, however, not related to exposure parameters. In both male and female Hg-exposed workers no significant disturbances were found in short-term memory (audioverbal), simple reaction time (visual), critical flicker fusion, and colour discrimination ability. Only slight renal tubular effects were detected in Hg-exposed males and females, ie, an increased urinary beta-galactosidase activity and an increased urinary excretion of retinol-binding protein. The prevalence of these preclinical renal effects was more related to the current exposure intensity (HgU) than to the duration of exposure and was detected mainly when HgU exceeds 50 micrograms/g creatinine. Changes in hand tremor spectrum recorded with an accelerometer were found in the Hg-exposed males only. The prevalence of abnormal values for some hand tremor parameters (total velocity and total displacement in the 2-50-Hz band) was mainly increased in male workers exposed for more than 10 yr. Unlike the renal tubular effects, the preclinical signs of tremor were more related to the integrated exposure than to the current exposure. Since the female workers, who have been exposed to Hg vapour levels usually insufficient to increase their HgU levels above 50 micrograms/g creatinine, did not exhibit any change in hand tremor pattern, the results of the present study tend to validate our previously proposed biological threshold limit value of a HgU of 50 micrograms/g creatinine for workers chronically exposed to mercury vapour.     

Biological aspects of occupational exposure to cadmium and several other metals

We have performed several cross-sectional epidemiological surveys among workers exposed to cadmium, mercury vapour or manganese in order to assess : their early biological or functional effects; the biological tests allowing an assessment of the amount of metal absorbed or stored in the body; the acceptable exposure levels. Studies have also been carried out among persons exposed to inorganic arsenic in order to define its inactivation mechanism and to develop a biological test of exposure. The kidney is the main critical organ following long-term exposure to cadmium. To prevent the occurrence of renal changes in the majority of male workers exposed to cadmium, its concentration in renal cortex should not exceed 215 micrograms/g (wet weight), and that in urine : 10 micrograms/g creatinine. A blood cadmium level of 1 microgram/100 ml has been suggested as maximum tolerable level for long-term exposure. Prolonged exposure to mercury vapour may lead to renal and neurological disturbances. The preclinical signs of nephrotoxicity are correlated with the amount of mercury absorbed which may be assessed by monitoring the mercury level in urine. The neurotoxic effects (particularly tremor) are mainly related to the integrated exposure (duration and intensity). A maximal permissible level of 50 micrograms Hg/g urinary creatinine is proposed to prevent the occurrence of these toxic effects. An exposure to manganese dust for 7 years on the average at a level below the maximum allowable airborne concentration (5 mg/m3) recommended by the ACGIH in the USA may still lead to a slight reduction in psychomotor and spirometric performances and interfere with calcium metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)     

Occupational mercury exposure and its consequences for behaviour

Summary Mercury is a known neurotoxin. Evidence from animal studies show behavioural impairment which can be long-lasting, after low-level exposure to mercury. Human research, however, has not been conclusive. Chronic, high-level mercury exposure such as occurred in Japan, and the Middle East, causes long-lasting and profound neurological damage. However the effects of low-level exposure, such as occurs in occupational exposure, are far from clear. This study used a comprehensive test battery based on an information processing framework to compare a group of twelve chronically mercury-exposed workers with a matched control group. The mercury-exposed group showed poorer psychomotor co-ordination and premature fatigue, although simple motor responses were not affected. General arousal levels also remained unaffected but mercury-exposed workers were superior in sustaining attention. In spite of this, the mercury-exposed group showed clear deficits in short-term memory.     

Effects of elemental mercury exposure at a thermometer plant

This study compares 84 mercury-exposed workers at a thermometer manufacturing facility with 79 unexposed workers for evidence of chronic mercury toxicity. Personal breathing-zone air concentrations of mercury ranged from 25.6 to 270.6 micrograms/m3 for thermometer workers. Urinary mercury levels in the study population ranged from 1.3 to 344.5 micrograms/g creatinine, with eight (10%) participants exceeding 150 micrograms/g creatinine and three workers exceeding 300 micrograms/g creatinine, which indicates increased absorption of mercury among the thermometer workers. All urine mercury levels in the comparison group were compatible with normal background levels in unexposed adults (less than 10 micrograms/g creatinine). Thermometer plant workers reported more symptoms than did controls; in general, these differences were not statistically significant and could not be specifically associated with mercury exposure. Static tremor, abnormal Romberg test, dysdiadochokinesia, and difficulty with heel-to-toe gait were more prevalent among thermometer workers than control workers, which could not be associated with recent mercury exposure; there was some suggestion of an association with chronic exposure. There were no intergroup differences for the standard clinical tests of renal function except for a significantly higher mean specific gravity among the thermometer workers. A positive correlation was found, however, between urinary N-acetyl-b-D-glucosaminidase (NAG) and urinary mercury. There was no consistent evidence for intergroup differences in proximal renal tubule function, as measured by urinary beta 2-microglobulin (B2M) or retinol binding protein (RBP).     

Chronic mercury exposure examined with a computer-based tremor system

Tremor is being increasingly evaluated by quantitative computer-based systems to differentiate its causes. In this study, a group of mercury-exposed workers were assessed to determine whether tremor characteristics differed by exposure level. Workers were classified into two groups: those with an average urine mercury concentration below the American Conference of Government Industrial Hygienist Biological Exposure Index of 35 micrograms/g creatinine, and those with an average urine mercury concentration above the Biological Exposure Index. Tremor characteristics (including intensity, harmonic index, center frequency, standard deviation of the center frequency, and tremor index) were measured and recorded with a computer-based tremor system. Sixteen of 17 workers who were potentially exposed to mercury participated in the study. Three workers had a mean urine mercury concentration of 27.0 micrograms/g-creatinine and were assigned to the low-exposure group, and 13 workers had a mean urine mercury concentration of 200.2 micrograms/g-creatinine and were assigned to the high-exposure group. There was a statistically significant difference in the tremor index (which compiles five individual tremor parameters into a single value) between the two groups (P = 0.04; Wilcoxon's rank sum test). Other tremor characteristics did not differ significantly between the groups. Tremor index may be more useful than measures of individual tremor parameters in differentiating normal from subclinical pathological tremors among groups of workers with chronic mercury exposure.     

Renal function and long-term low mercury vapor exposure

Renal function indicated by urinary albumin and N-acetyl-beta-glucosaminidase was studied among a group of male chlorine-alkali workers (N = 60) and their matched referents (N = 60). Exposure to mercury vapor had occurred at least 5 y (mean 13.7 y; SD 5.5 y). The estimated long-term exposure level calculated from the time-weighted average blood concentrations of mercury had been approximately 25 micrograms/m3 of air. Neither glomerular nor tubular effects were shown in the exposed workers.     

Psychological performance and long-term exposure to mercury vapors

In a cross-sectional study the psychological test performances of a group of 36 male chlorine-alkali workers were compared with the level of exposure to mercury and to the corresponding results of referents. The mercury exposure had lasted for at least 10 years and had been controlled by regular health examinations and urine analyses. Several dose indicators were calculated. The more heavily exposed workers performed more poorly on the verbal intelligence test (Similarities) than the referents did. Impairments in the memory tests showed a statistically significant correlation with the actual exposure level, especially with the actual concentration of mercury in blood. The monitoring of mercury in blood can be useful in health surveillance programs. The level of mercury in the air was calculated from the dose indicators. The results support the recommended exposure limit of 25 micrograms/m3 for metallic mercury vapor in the air as a level avoiding adverse effects in exposed workers.     

Evaluation of the neurotoxic and nephrotoxic effects following long-term exposure to metallic mercury in employed at a chlorine/sodium-hydroxide plant

OBJECTIVES: Within the frame work of a wide multicentre study, a sub-study was developed in order to explore the occurrence of early effects on the central nervous system, on the kidney and on the neuro-immune system in the workers of a chloro-alkali production plant exposed to metallic mercury at airborne concentration levels lower than 0.025 mg/m3 (TLV-TWA). They were compared to a control population of employees of the same huge petrochemical plant with different job that did not implicate exposure to mercury vapors. Specifically, the study aimed at revealing the occurrence of early effects on the central nervous system related with mercury exposure, as can be assessed through neurophysiological and neurobehavioral tests. METHODS: The excretion of urinary mercury was measured by atomic absorption spectrometry. The study of renal function was assessed by measurement of the urinary excretion of some high and low molecular weight protein markers (albumin, beta 2-microglobulin, retinol-binding protein, fibronectin, specific proximal tubule brush border antigens, N-acetyl-beta-D-glucosaminidase). The neurobehavioral status of the study subjects was assessed by means of several test parameters (Simple Reaction Time, Color Word Vigilance Test, Symbol Digit, Finger Tapping, Mood Scale of Kjellberg and Iwanowski, Subjective symptoms questionnaire (QSS), Luria Nebraska Motor Scale, Branches Alternate Movement Task and Tremometry). RESULTS: The values of urinary excretion averaged 12 +/- 8 micrograms Hg/g of creatinine for the exposed workers group (n = 38), while for the reference group (n = 34 cases) urinary excretion was statistically lower, averaging 4 +/- 6 micrograms Hg/g of creatinine. Neither the parameters selected for the assessment of renal functions, nor those chosen to probe the neurobehavioral status of the probands revealed statistically reliable differences between the group of exposed workers (length of exposure: range 1-34 years) and the control group. Nevertheless, some minor but still statistically reliable correlations were found between some neurobehavioral parameters and some demographic variables describing the whole group of tested workers, but not to the level of occupational exposure to mercury. CONCLUSIONS: The results of the study confirm the lack of toxic effects of clinical importance on the central nervous system and on the kidney for values of mercury urinary excretion lower than the suggested index of biological exposure (IBE) of 35 micrograms Hg/gram of creatinine.     

Urinary kallikrein activity in workers exposed to cadmium, lead, or mercury vapour.

A significant reduction of kallikrein activity in urine (assayed by its amidolytic activity) was found in 64 normotensive workers who had been exposed to cadmium for 11 years on average and whose cadmium concentrations in urine ranged from 2.2 to 33.1 micrograms/g creatinine. The mean (geometric) urinary kallikrein activity (in U/g creatinine) amounted to 0.52 (range 0.11-1.90) in the control group (n = 193) against 0.39 (range 0.10-1.03) in the cadmium group, and the prevalence of abnormally low activity levels (less than or equal to 0.20 U/g creatinine) amounted to 17.2% in the cadmium group against 5.2% in the control group. A reduction of aldosterone release (aldosterone in urine) associated with an increased natriuresis was also observed. This might constitute a compensatory mechanism maintaining blood pressure in the normal range. These biological effects of cadmium were not reversible after removal from exposure. This study indicates that cadmium can induce an irreversible toxic effect in the distal nephron. It also suggests that an excessive cadmium body burden alone may not be sufficient to induce hypertension, but in individuals whose blood pressure regulation may be impaired by other factors cadmium could stimulate the development of hypertension. This study also supports the recommendation to prevent hypertensive subjects from being exposed to cadmium. There was no indication that moderate exposure to mercury vapour (n = 53; mercury in urine, range 11-224 micrograms/g creatinine; average duration of exposure: six years) or to inorganic lead (n = 23; lead in blood, range 40-67 micrograms/100 ml; average duration of exposure: eight years) was associated with a reduction of kallikrein production by the kidney.     

Urinary kallikrein activity in workers exposed to cadmium, lead, or mercury vapour

A significant reduction of kallikrein activity in urine (assayed by its amidolytic activity) was found in 64 normotensive workers who had been exposed to cadmium for 11 years on average and whose cadmium concentrations in urine ranged from 2.2 to 33.1 micrograms/g creatinine. The mean (geometric) urinary kallikrein activity (in U/g creatinine) amounted to 0.52 (range 0.11-1.90) in the control group (n = 193) against 0.39 (range 0.10-1.03) in the cadmium group, and the prevalence of abnormally low activity levels (less than or equal to 0.20 U/g creatinine) amounted to 17.2% in the cadmium group against 5.2% in the control group. A reduction of aldosterone release (aldosterone in urine) associated with an increased natriuresis was also observed. This might constitute a compensatory mechanism maintaining blood pressure in the normal range. These biological effects of cadmium were not reversible after removal from exposure. This study indicates that cadmium can induce an irreversible toxic effect in the distal nephron. It also suggests that an excessive cadmium body burden alone may not be sufficient to induce hypertension, but in individuals whose blood pressure regulation may be impaired by other factors cadmium could stimulate the development of hypertension. This study also supports the recommendation to prevent hypertensive subjects from being exposed to cadmium. There was no indication that moderate exposure to mercury vapour (n = 53; mercury in urine, range 11-224 micrograms/g creatinine; average duration of exposure: six years) or to inorganic lead (n = 23; lead in blood, range 40-67 micrograms/100 ml; average duration of exposure: eight years) was associated with a reduction of kallikrein production by the kidney.     

Evaluation of the dose of mercury in exposed and control subjects

OBJECTIVES: The aim of this paper was to analyse the concentrations of HgU and HgB in three different groups: 122 workers exposed, 18 workers formerly exposed and 196 subjects not occupationally or environmentally exposed to mercury. METHODS: All the subjects filled out a questionnaire concerning personal data, lifestyle, occupational or non-occupational exposure to Hg and medical history. The amalgam fillings area was measured by a standardised method. RESULTS: Urinary mercury excretion was significantly greater in the group of the exposed workers respect to the group of subjects not occupationally exposed (Median value of 8.3 micrograms/g creatinine and the 5 degrees and 95 degrees percentile respectively of 2.66 e 23.50 micrograms/g creatinine against Median value of 1.2 micrograms/g creatinine and the 5 degrees and 95 degrees percentile respectively of 0.18 and 5.42 micrograms/g creatinine). U-Hg in formerly exposed workers were comparable to U-Hg in non-occupationally exposed subjects, with a median value of 1.6 micrograms/g creatinine. B-Hg values were similar in the three groups: the median value was 3.1 micrograms/l in the non-occupationally exposed, 4.0 micrograms/l in the exposed workers and 3.9 micrograms/l in the past exposed. These value were not significantly different. Among the considered variables (amalgam fillings, fish consumption, age, sex, alcohol intake, chewing-gum and smoking) dental amalgam and fish consumption were significantly related with the Hg urinary excretion and the B-Hg levels. This is particularly true considering the subjects altogether: for the exposed workers, indeed, the occupational exposure was the most relevant variable. CONCLUSIONS: The results of the present research confirmed that the U-Hg excretion in non-occupationally exposed subjects is influenced by amalgam dental fillings. Furthermore, in our study Hg urinary excretion was significantly related with fish consumption. This fact can be explained, according to several recent experimental human and animal trials, considering that methylmercury contained in fish is partially converted, through breakage of the carbon-Hg bond, into Hg inorganic forms, which accumulate in the kidney and have a urinary excretion pathway.     

An evaluation of renal function in workers occupationally exposed to mercury vapour

The renal function of a population of workers occupationally exposed to mercury in the chlor-alkali industry has been examined and compared to that of a population of workers with no occupational exposure to mercury. Measurement of specific urinary proteins and enzymes have been carried out on each individual on three separate occasions and have been complemented by blood plasma measurements at the final visit. Under the conditions of exposure to mercury sustained in this study, there is no evidence of an increased prevalence of renal dysfunction as indicated by enzyme and protein measurements. The urinary concentration of the low molecular weight protein, beta 2-microglobulin, is significantly lower in the mercury-exposed group than in the control group. In contrast to recently published literature, no relationship is seen between urinary mercury concentration and the appearance of high molecular weight protein in urine. A small increase in the prevalence of higher activities of the urinary enzyme N-acetyl-beta-glucosaminidase and gamma glutamyl transferase is observed when the urinary mercury concentration exceeds 100 micrograms/g creatinine. A small increase in the prevalence of raised urinary N-acetyl-beta-glucosaminidase activity is observed when the duration of exposure to mercury exceeds ten years. The pattern of proteinuria has been characterised in a total of sixteen individuals from both populations; a low molecular weight proteinuria is seen in three individuals from the control group whilst a high molecular weight proteinuria is seen in the remainder (seven in the control and six in the mercury group).     

Effects of low exposure to inorganic mercury on psychological performance

The effects of low exposure to inorganic mercury on psychological performance was investigated: the study groups included eight chronically exposed workers and 20 who were only occasionally exposed. These were compared with a control group of 22 subjects from the same plant who were not exposed to mercury. All subjects were administered the WHO test battery to detect preclinical signs of central nervous system impairment: the battery includes the Santa Ana (Helsinki version) test, simple reaction time, the Benton test, and the Wechsler digit span and digit symbol. In addition, the Gordon test was used to study personality profiles and the clinical depression questionnaire. Urinary mercury was used as indicator for internal dose. To this effect, urinary mercury observed in workers examined from 1979 to 1987 was evaluated. Of the pyschic functions explored by behavioural tests, only short term auditory memory was found to be impaired in the chronically exposed workers (p less than 0.05 compared with the controls). The chronically exposed workers were also found to be more depressed than those in the two other groups. No changes of visual motor functions were observed. The personality of the occupationally exposed workers was found to be considerably changed compared with that of the control group. On the basis of the results obtained and in view of urinary mercury mean concentrations in the exposed group which were 30-40 micrograms/l over the years, it is suggested that the TLV-TWA for mercury should be lowered to 0.025 mg/m3 and that the biological urinary exposure indicator for biological monitoring should be 25 micrograms/l.     

Effects of low exposure to inorganic mercury on psychological performance.

The effects of low exposure to inorganic mercury on psychological performance was investigated: the study groups included eight chronically exposed workers and 20 who were only occasionally exposed. These were compared with a control group of 22 subjects from the same plant who were not exposed to mercury. All subjects were administered the WHO test battery to detect preclinical signs of central nervous system impairment: the battery includes the Santa Ana (Helsinki version) test, simple reaction time, the Benton test, and the Wechsler digit span and digit symbol. In addition, the Gordon test was used to study personality profiles and the clinical depression questionnaire. Urinary mercury was used as indicator for internal dose. To this effect, urinary mercury observed in workers examined from 1979 to 1987 was evaluated. Of the pyschic functions explored by behavioural tests, only short term auditory memory was found to be impaired in the chronically exposed workers (p less than 0.05 compared with the controls). The chronically exposed workers were also found to be more depressed than those in the two other groups. No changes of visual motor functions were observed. The personality of the occupationally exposed workers was found to be considerably changed compared with that of the control group. On the basis of the results obtained and in view of urinary mercury mean concentrations in the exposed group which were 30-40 micrograms/l over the years, it is suggested that the TLV-TWA for mercury should be lowered to 0.025 mg/m3 and that the biological urinary exposure indicator for biological monitoring should be 25 micrograms/l.     

Urinary excretion of mercury after occupational exposure to mercury vapour and influence of the chelating agent meso-2,3-dimercaptosuccinic acid (DMSA).

The spontaneous and chelator mediated excretion of mercury in urine was investigated in male subjects occupationally exposed to mercury vapour (alkaline battery and chloralkali plants) who did not exhibit any sign of kidney damage. The time course of the spontaneous elimination of mercury in urine was examined in seven workers (age 22-40) who had been removed from exposure to mercury vapour (average duration of exposure 4.4 years) because their urinary mercury concentrations repeatedly exceeded 100 micrograms/g creatinine. The post exposure observation period started 10 to 29 days after the date of removal and lasted about 300 days (slow HgU elimination phase). For each worker, the kinetics of the spontaneous HgU decline followed a first order process; the biological half life ranged from 69 to 109 days (mean 90 days). The increased urinary excretion of mercury after a single oral administration of 2 g meso-2,3-dimercaptosuccinic acid (DMSA) was investigated in 16 control workers (group A; age 23 to 49), in 11 workers removed from exposure for at least two years (group B; age 27 to 41), and in 16 workers currently exposed to mercury vapour (group C; age 21 to 58). In group C, the DMSA experiment was repeated twice (three weeks before and three weeks after a holiday) after measures had been taken to reduce the mercury emission. The urinary mercury excretion was significantly higher during the 24 hours after DMSA administration in all groups compared with that in the 24 hours before. The bulk (50-70%) of the DMSA stimulated mercury excretion appeared within the first eight hours. In each group, the amount of mercury (microgram Hg/24h) excreted after DMSA was significantly correlated with that before administration of DMSA. The groups whose exposure had ceased, however, exhibited much higher correlation for coefficients (r=0.97 for group B and 0.86 for group C after three weeks of holiday) than those currently exposed to mercury vapour (r-0.66 for group C before and 9.58 after reduction of exposure). The data suggest that after a few days of cessation of occupational exposure to mercury vapour the HgU before and after administration of DMSA mainly reflects the amount of mercury stored in the kidney, which represents a mercury pool with a slow turnover.     

Urinary excretion of mercury after occupational exposure to mercury vapour and influence of the chelating agent meso-2,3-dimercaptosuccinic acid (DMSA).

The spontaneous and chelator mediated excretion of mercury in urine was investigated in male subjects occupationally exposed to mercury vapour (alkaline battery and chloralkali plants) who did not exhibit any sign of kidney damage. The time course of the spontaneous elimination of mercury in urine was examined in seven workers (age 22-40) who had been removed from exposure to mercury vapour (average duration of exposure 4.4 years) because their urinary mercury concentrations repeatedly exceeded 100 micrograms/g creatinine. The post exposure observation period started 10 to 29 days after the date of removal and lasted about 300 days (slow HgU elimination phase). For each worker, the kinetics of the spontaneous HgU decline followed a first order process; the biological half life ranged from 69 to 109 days (mean 90 days). The increased urinary excretion of mercury after a single oral administration of 2 g meso-2,3-dimercaptosuccinic acid (DMSA) was investigated in 16 control workers (group A; age 23 to 49), in 11 workers removed from exposure for at least two years (group B; age 27 to 41), and in 16 workers currently exposed to mercury vapour (group C; age 21 to 58). In group C, the DMSA experiment was repeated twice (three weeks before and three weeks after a holiday) after measures had been taken to reduce the mercury emission. The urinary mercury excretion was significantly higher during the 24 hours after DMSA administration in all groups compared with that in the 24 hours before. The bulk (50-70%) of the DMSA stimulated mercury excretion appeared within the first eight hours. In each group, the amount of mercury (microgram Hg/24h) excreted after DMSA was significantly correlated with that before administration of DMSA. The groups whose exposure had ceased, however, exhibited much higher correlation for coefficients (r=0.97 for group B and 0.86 for group C after three weeks of holiday) than those currently exposed to mercury vapour (r-0.66 for group C before and 9.58 after reduction of exposure). The data suggest that after a few days of cessation of occupational exposure to mercury vapour the HgU before and after administration of DMSA mainly reflects the amount of mercury stored in the kidney, which represents a mercury pool with a slow turnover.     

Neurotoxic effect of exposure to low doses of mercury

OBJECTIVES: To assess early effects on the Central Nervous System due to occupational exposure to low levels of inorganic mercury (Hg) in a multicenter nationwide cross-sectional study, including workers from chloro-alkali plants, chemical industry, thermometer and fluorescent lamp manufacturing. The contribution of non-occupational exposure to inorganic Hg from dental amalgams and to organic Hg from fish consumption was also considered. METHODS: Neuropsychological and neuroendocrine functions were examined in a population of 122 workers occupationally exposed to Hg, and 196 control subjects, not occupationally exposed to Hg. Neuropsychological functions were assessed with neurobehavioral testing including vigilance, motor and cognitive function, tremor measurements, and with symptoms concerning neuropsychological and mood assessment. Neuroendocrine functions were examined with the measurement of prolactin secretion. The target population was also characterized by the surface of dental amalgams and sea fish consumption. RESULTS: In the exposed workers the mean urinary Hg (HgU) was 10.4 +/- 6.9 (median 8.3, geometric mean 8.3, range 0.2-35.2) micrograms/g creatinine, whereas in the control group the mean HgU was 1.9 +/- 2.8 (median 1.2, geometric mean 1.2, range 0.1-33.2) micrograms/g creatinine. The results indicated homogeneous distribution of most neurobehavioral parameters among exposed and controls. On the contrary, finger tapping (p < 0.01) and the BAMT (Branches Alternate Movement Task) coordination test (p = 0.05) were associated with occupational exposure, indicating an impairment in the exposed subjects. Prolactin levels resulted significantly decreased among the exposed workers, and inversely related to HgU on an individual basis (p < 0.05). An inverse association was also observed between most neuropsychological symptoms and sea fish consumption, indicating a "beneficial effect" from eating sea fish. On the contrary, no effects were observed as a function of dental amalgams. CONCLUSIONS: In conclusion, this study supports the finding of early alterations of motor function and neuroendocrine secretion at very low exposure levels of inorganic Hg, below the current ACGIH BEI and below the most recent exposure levels reported in the literature.     

Endocrine function in mercury exposed chloralkali workers.

OBJECTIVE--The aim was to study whether functional impairment of the pituitary, thyroid, testes, and adrenal glands of humans occupationally exposed to mercury (Hg) vapour can be shown as a result of accumulation of Hg in these glands. METHODS--Basal concentrations of thyrotrophin (TSH), prolactin, free thyroxine (free T4), free 3,5,3'-triiodothyronine (free T3), antibodies against thyroperoxidase, and testosterone in serum, as well as cortisol in morning urine were measured in 41 chloralkali workers exposed (10 years on average) to Hg vapour, and in 41 age matched occupationally unexposed referents. The chloralkali workers had a mean urinary Hg concentration (U-Hg) of 15 nmol/mmol (27 micrograms/g) creatinine, and a mean blood Hg concentration (B-Hg) of 46 nmol/l. For the reference group U-Hg and B-Hg were 1.9 nmol/mmol (3.3 micrograms/g) creatinine and 17 nmol/l respectively. RESULTS--The serum free T4 concentration and the ratio free T4/free T3 were slightly, but significantly, higher in the subgroups with the highest exposure, and the serum free T3 was inversely associated with cumulative Hg exposure. This indicates a possible inhibitory effect of mercury on 5'-deiodinases, which are responsible for the conversion of T4 to the active hormone T3. Serum total testosterone, but not free testosterone, was positively correlated with cumulative Hg exposure. Prolactin, TSH and urinary cortisol concentrations were not significantly associated to exposure. CONCLUSION--Apart from inhibition of the deiodination of T4 to T3, the endocrine functions studied seem not to be affected by exposure to Hg vapour at the exposure levels of the present study. Growth hormone secretion was not studied.     

Renal and immunological effects of occupational exposure to inorganic mercury.

Seven parameters of renal dysfunction (urinary excretion of albumin, orosomucoid, beta 2-microglobulin, N-acetyl-beta-glucosaminidase (NAG), and copper; serum creatinine concentration, and relative clearance of beta 2-microglobulin) were examined in a group of chloralkali workers exposed to mercury vapour (n = 89) and in an unexposed control group (n = 75). Serum concentrations of immunoglobulins (IgA, IgG, IgM) and auto-antibodies towards glomeruli and other tissues were also determined. The parameters examined were compared between the two groups and related to different exposure parameters. In the chloralkali group median blood mercury concentration (B-Hg) was 55 nmol/l, serum mercury (S-Hg) 45 nmol/l, and urine mercury concentration (U-Hg) 14.3 nmol/mmol creatinine (25.4 micrograms/g creatinine). Corresponding concentrations for the control group were 15 nmol/l, 4 nmol/l, and 1.1 nmol/mmol creatinine (1.9 micrograms/g creatinine) respectively. None of the parameters of renal dysfunction differed significantly between the two groups, but there was a tendency to increased excretion of NAG in the exposed group compared with the controls. Also, a statistically significant relation existed between U-Hg and U-NAG (p less than 0.001). Serum immunoglobulin concentrations did not differ between the groups, and serum titres of autoantibodies (including antiglomerular basement membrane and antilaminin antibodies) were low in both groups. Thus the results gave no evidence of glomerular damage or of a tubular reabsorption defect at the current relatively low exposures. The findings still indicate slight, dose related tubular cell damage in the mercury exposed group. There were no signs of a mercury induced effect on the immune system.