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.     

Effects of occupational exposure to mercury vapour on the central nervous system.

Possible effects of mercury on the central nervous system (CNS) were examined in a group of chloralkali workers exposed to mercury (n = 89) and compared with a control group (n = 75), by registration of subjective symptoms, personality changes, forearm tremor, and performance on six computerised psychometric tests in the two groups. The groups were similar in age, education, verbal comprehension, and work tasks. In the chloralkali group, median blood mercury concentration (B-Hg) was 55 nmol/l, serum mercury concentration (S-Hg) 45 nmol/l, and urine mercury concentration (U-Hg) 14.3 nmol/mmol creatinine (25.4 micrograms/g creatinine). Corresponding concentrations in the control group were 15 nmol/l, 4 nmol/l, and 1.1 nmol/mmol creatinine (1.9 micrograms/g creatinine) respectively. The number of self reported symptoms, the scores for tiredness and confusion in the profile of mood states (POMS), and the degree of neuroticism in the Eysenck personality inventory (EPI), were significantly higher in the mercury exposed group compared with the controls. Performance on the psychometric tests and tremor frequency spectra did not differ significantly between the two groups. Dose-response calculations showed weak but statistically significant relations between symptom prevalence and current mercury concentrations in both blood and urine. The performance on three of the psychometric tests was negatively correlated with earlier peak exposures. The findings indicate a slight mercury induced effect on the CNS among the chloralkali workers.     

Effects of occupational exposure to mercury vapour on the central nervous system.

Possible effects of mercury on the central nervous system (CNS) were examined in a group of chloralkali workers exposed to mercury (n = 89) and compared with a control group (n = 75), by registration of subjective symptoms, personality changes, forearm tremor, and performance on six computerised psychometric tests in the two groups. The groups were similar in age, education, verbal comprehension, and work tasks. In the chloralkali group, median blood mercury concentration (B-Hg) was 55 nmol/l, serum mercury concentration (S-Hg) 45 nmol/l, and urine mercury concentration (U-Hg) 14.3 nmol/mmol creatinine (25.4 micrograms/g creatinine). Corresponding concentrations in the control group were 15 nmol/l, 4 nmol/l, and 1.1 nmol/mmol creatinine (1.9 micrograms/g creatinine) respectively. The number of self reported symptoms, the scores for tiredness and confusion in the profile of mood states (POMS), and the degree of neuroticism in the Eysenck personality inventory (EPI), were significantly higher in the mercury exposed group compared with the controls. Performance on the psychometric tests and tremor frequency spectra did not differ significantly between the two groups. Dose-response calculations showed weak but statistically significant relations between symptom prevalence and current mercury concentrations in both blood and urine. The performance on three of the psychometric tests was negatively correlated with earlier peak exposures. The findings indicate a slight mercury induced effect on the CNS among the chloralkali workers.     

Biological monitoring of environmental and occupational exposure to mercury

Summary Biological monitoring was used to assess mercury exposure from occupational and environmental sources in a group of chloralkali workers (n = 89) and in a control group (n = 75). In the control group, the median value for blood mercury (B-Hg) was 15 nmol/l, that for serum mercury (S-Hg) was 4 nmol/l and that for urinary mercury (U-Hg) was 1.1 nmol/mmol creatinine. Corresponding levels in the chloralkali group were 55 nmol/l, 45 nmol/l and 14.3 nmol/mmol creatinine, respectively. In the control group, there were statistically significant relationships between fish consumption and both B-Hg and S-Hg values (P < 0.001), whereas U-Hg correlated best with the individual amalgam burden (P < 0.01). In the chloralkali group, the mercury levels in blood and urine were significantly related to the type of work (P < 0.001) but not to the length of employment, to fish consumption or to the quantity of dental amalgam fillings. In both groups there were poor correlations between smoking or alcohol intake and the mercury levels in blood and urine. The results strongly suggest that fish is an important source of methylmercury exposure and that amalgam fillings are probably the most important source of inorganic mercury exposure among occupationally unexposed individuals. In the chloralkali group, mercury exposure from fish and amalgam was overshadowed by occupational exposure to inorganic mercury.     

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.     

Assessment of renal dysfunction in workers previously exposed to mercury vapour at a chloralkali plant.

Urinary albumin concentration (U-alb) and N-acetyl-beta-D-glucosaminidase (U-NAG) and glomerular basement membrane antibodies (a-GBMs) in serum samples were measured in 77 chloralkali workers previously exposed to mercury (Hg) vapour and 53 age matched referents. The exposure ceased on average 12.3 (range 1-35) years before the study. The mean exposure time was 7.9 (range 1.1-36.2) years. The mean yearly urinary Hg concentration (U-Hg) was 531 nmol/l. The concentrations of the urinary isoenzymes NAG A (U-NAG A) and NAG B (U-NAG B) were determined in 30 highly exposed subjects and 30 referents. No differences in U-alb or U-NAG, U-NAG A, or U-NAG B were found between the groups. Higher concentrations of a-GBMs were found among subjects who stopped exposure a short time before the study, but there was no association between a-GBMs and U-alb. The U-NAG and U-NAG A were negatively correlated with storage time. The results may suggest that microalbuminuria and enzymuria reported in subjects with ongoing exposure to Hg vapour are reversible in most instances.     

Renal tubular function of workers exposed to low levels of cadmium.

Cadmium induced renal tubular effects were examined in 65 female workers in a factory manufacturing nickel cadmium batteries. Urinary beta 2-microglobulin (beta 2m), urinary N-acetyl-D-glucosaminidase activity (NAG), and serum creatinine and serum urea concentrations were used to assess the renal effects. Of the four measures, only urinary NAG and urinary beta 2m showed a strong positive correlation with blood cadmium concentrations (r = 0.49 and 0.43 respectively); NAG showed a weaker correlation with urinary cadmium concentrations (r = 0.35). Urinary beta 2m has weak correlation with urinary cadmium (r = 0.04). Only urinary NAG showed a significant deterioration in renal function among the exposed group. NAG detects the largest proportion of abnormalities among the exposed group. Abnormal urinary beta 2m is detected in only 15.4% of the workers, half of whom have blood cadmium above 10 micrograms/l. The proportion of abnormalities detected by urinary NAG differs significantly from the proportion of abnormalities detected by urinary beta 2m (p less than 0.01). The age adjusted mean urinary NAG excretion showed a significant rise with urinary cadmium of above 3 micrograms/g creatinine. Urinary beta 2m failed to show any significant rise. With blood cadmium concentrations, the age adjusted mean urinary NAG excretion showed a rise from 1 microgram/l of blood cadmium followed by a plateau between blood cadmium concentrations of 3-10 micrograms/l. No significant rise in mean urinary excretion in beta 2m was seen until blood cadmium concentrations exceeded 10 micrograms/l.     

Renal tubular function of workers exposed to low levels of cadmium

Cadmium induced renal tubular effects were examined in 65 female workers in a factory manufacturing nickel cadmium batteries. Urinary beta 2-microglobulin (beta 2m), urinary N-acetyl-D-glucosaminidase activity (NAG), and serum creatinine and serum urea concentrations were used to assess the renal effects. Of the four measures, only urinary NAG and urinary beta 2m showed a strong positive correlation with blood cadmium concentrations (r = 0.49 and 0.43 respectively); NAG showed a weaker correlation with urinary cadmium concentrations (r = 0.35). Urinary beta 2m has weak correlation with urinary cadmium (r = 0.04). Only urinary NAG showed a significant deterioration in renal function among the exposed group. NAG detects the largest proportion of abnormalities among the exposed group. Abnormal urinary beta 2m is detected in only 15.4% of the workers, half of whom have blood cadmium above 10 micrograms/l. The proportion of abnormalities detected by urinary NAG differs significantly from the proportion of abnormalities detected by urinary beta 2m (p less than 0.01). The age adjusted mean urinary NAG excretion showed a significant rise with urinary cadmium of above 3 micrograms/g creatinine. Urinary beta 2m failed to show any significant rise. With blood cadmium concentrations, the age adjusted mean urinary NAG excretion showed a rise from 1 microgram/l of blood cadmium followed by a plateau between blood cadmium concentrations of 3-10 micrograms/l. No significant rise in mean urinary excretion in beta 2m was seen until blood cadmium concentrations exceeded 10 micrograms/l.     

Mercury and selenium in workers previously exposed to mercury vapour at a chloralkali plant.

The concentrations of total mercury (B-Hg), inorganic mercury (B-IHg), and methyl mercury (B-MeHg) in whole blood, urinary mercury (U-Hg), and selenium in urine (U-Se) and whole blood (B-Se) were determined in 74 chloralkali workers previously exposed to Hg vapour, and compared with 51 age matched referents. Dental amalgam state, fish consumption, and exposure related indices were studied with regard to the determined elements. A significant relation between the surface of dental amalgam and U-Hg (Pearson's r = 0.63, p < 0.001) was found among the referents. Mean U-Se was significantly lower (p < 0.001) among the subjects previously exposed to Hg (34.1 nmol/mmol creatinine) compared with that for the referents (42.6 nmol/mmol creatinine). A significant negative relation between the cumulative Hg dose and U-Se was also found. The mechanisms and the clinical significance of these findings are not clear. No relation between current U-Hg and previous occupational exposure to Hg was found among subjects in whom exposure had ceased more than one year before the study.     

A study of autoantibodies and circulating immune complexes in mercury-exposed chloralkali workers

Inorganic mercury may cause immunologically mediated disease: e.g., glomerulonephritis, acrodynia, and contact allergy. Animal models have demonstrated the importance of genetic factors in determining susceptibility and resistance to autoimmunity, as well as the specific manifestation of the autoimmune response. Findings in groups of workers with occupational exposure to inorganic mercury have been inconsistent. Objective: To investigate whether an immune response, caused by exposure to inorganic mercury (Hg), could be shown in occupationally exposed workers. Methods: Immunoglobulin G (IgG), antinuclear autoantibodies, antibodies against thyroid, stomach or kidney antigens using indirect immunofluorescence, antibodies against glomerular basement membrane using ELISA, and circulating immune complexes in serum, and albumin in urine, were examined in Hg-exposed workers and controls. The two groups, 41 male chloralkali workers exposed to Hg vapour (mean exposure time 9 years) and 41 unexposed controls were age-matched and recruited from the same company. Hg concentrations in whole blood (B-Hg), plasma (P-Hg), and urine (U-Hg) were determined using cold vapor atomic spectrometry. Design: Cross-sectional study. Results: The mean B-Hg, P-Hg and U-Hg levels were 46 nmol/l, 37 nmol/l, and 27 μg/g creatinine in the exposed group, and 17 nmol/l, 6.9 nmol/l, and 3.4 μg/g creatinine in the referents. No statistically significant differences were found regarding IgG levels, urinary albumin excretion, prevalence of abnormal titers of autoantibodies or circulating immune complexes. There were no statistically significant associations between autoantibodies or immune complexes on the one hand and mercury exposure indices on the other. Conclusion: The results indicate that, if and when lasting autoimmune response occurs at the mercury exposure levels of the present study, it is uncommon. A small fraction of humans may, however, be susceptible to the development of autoimmunity, and there is also a possible “healthy worker” selection. Thus cross-sectional studies of moderate numbers of active workers will have low power to demonstrate autoimmune effects. Received: 2 September 1996 / Accepted: 3 January 1997     

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.     

Effects of occupational exposure to mercury vapor on lymphocyte micronuclei

For 26 chloralkali workers exposed to inorganic mercury and 26 age-matched, occupationally unexposed referents, the frequency and size distribution of micronuclei were determined in peripheral lymphocytes stimulated with either phytohemagglutinin or pokeweed mitogen. For the exposed workers the mean concentrations of mercury in urine, plasma, and erythrocytes were 16 nmol/mmol of creatinine, 48 nmol/l, and 78 nmol/l, respectively, and their mean exposure time was 10 years. Neither the frequency nor the size of micronuclei was significantly different in the two groups; nor were there any correlations to current mercury levels. However, in the exposed group, and with phytohemagglutinin as the mitogen, a statistically significant correlation between previous exposure to mercury (cumulative exposure or number of blood mercury peaks) and the frequency of micronuclei was found. This association was also present when the effects of age and smoking were allowed for, and it may indicate an accumulation of cytogenetic effects in T-lymphocytes.     

Mercury in the Swedish chloralkali industry--an evaluation of the exposure and preventive measures over 40 years

The monitoring of exposure to mercury in the Swedish chloralkali industry started in 1946 and became common in the 1960s. During the 1970s both urinary and blood mercury (U-Hg, B-Hg) concentrations decreased substantially. The mean (geometric) U-Hg was 500-700 nmol l.-1 in the 1960s as compared with 150 nmol l.-1 today. During the 1970s the mean (geometric) B-Hg declined from about 100 to 40 nmol l.-1. Nowadays high values, U-Hg greater than 1500 nmol l.-1 or B-Hg greater than 600 nmol l.-1, are very rare whereas in the 1950s and the 1960s such peak values were found among 30% of the workers. The most effective measures taken were the reduction of the hydrogen discharges from the process and the replacement of graphite anodes by dimensionally stable anodes which require less frequent maintenance. Today efficient cleaning and continuous monitoring make it possible to keep the exposure levels low. The use of respiratory protection equipment is, however, still necessary during certain maintenance operations.     

Decrease in mercury concentration in blood after long term exposure: a kinetic study of chloralkali workers.

The elimination of mercury (Hg) in blood was investigated in 14 chloralkali workers exposed to metallic Hg vapour for 1-24 (median 10) years. Blood and urine samples were collected on several (median eight) occasions during a period of 17-26 days. The initial Hg concentrations were about 80 nmol/l in whole blood (B-Hg) and 17 nmol/mmol creatinine in urine (U-Hg). The decrease in Hg in whole blood, plasma (P) and erythrocytes (Ery) was best characterised by a two compartment model. In a model with a common half life for all subjects, the best fit for B-Hg was obtained with half lives of 3.8 days for a fast phase and 45 days for a slow phase. The half life of the fast phase was shorter for P-Hg than for Ery-Hg, whereas the opposite was the case for the slow phase. The half lives of the slow phases in whole blood and plasma were longer, and the relative fractions of the slow phases were higher (about 50%) after long term exposure than those (about 20%) reported after brief exposure. Slower elimination indicates higher accumulation of Hg in organs with long half lives, and possibly the presence of at least one additional, even slower compartment. The U-Hg fluctuated substantially during the sampling period, and average concentrations decreased only slightly.     

Minimal immunological effects on workers with prolonged low exposure to inorganic mercury.

OBJECTIVES: This study was carried out to investigate possible immunological changes in workers with prolonged low exposure to inorganic mercury in a fluorescent light bulb factory. METHODS: 29 immunological variables were examined in 34 workers with prolonged low level exposure to inorganic mercury (exposed workers) and 35 unexposed workers as the controls. The selected indicator of mercury exposure was concentration of mercury in the urine (U-Hg), which declined progressively from 36.0 micrograms/l in 1978 to 6.0 micrograms/l in the study year 1994. RESULTS: None of the exposed workers had ever shown signs of either acute or chronic inorganic mercury toxicity or had shown any form of hypersensitivity. The only changes found in the exposed workers, compared with the controls, were a reduction of the cells that express cluster differentiation (CD25,(T activation antigen (Tac antigen))) and concentrations of tumour necrosis factor-alpha (TNF-alpha) in serum. However, the decrease of cells that express CD25 was unrelated to occupational exposure and was, in all likelihood a chance finding. Conversely, the decline in serum TNF-alpha was closely associated with occupational exposure. However, no dose-response relation was found between U-Hg and TNF-alpha concentrations; nor were TNF-alpha concentrations affected by cumulative occupational exposure to inorganic mercury in over 20 years. CONCLUSIONS: Tentatively, we suggest that reduced serum TNF-alpha concentrations might be indicative of an in vivo functional defect of the monocyte macrophage system in this particular group of workers even though they were clinically asymptomatic.     

Significance of biological indicators of mercury exposure

BACKGROUND: It was considered appropriate to update of the significance and use of the different mercury exposure indicators. OBJECTIVE: The aim of the this paper was to correctly select biological media and sampling time and to understand the toxic kinetics of mercury for assessment of accurate biological monitoring. RESULTS: It was confirmed that mercury in blood (B-Hg) is a good indicator of recent exposure, while urinary mercury (U-Hg) indicates current exposure when mercury reaches the renal steady state. B-Hg values are greatly influenced by fish consumption, while the variables influencing U-Hg values are amalgam fillings, commercial gamma-globulin preparations, vaccines, topical remedies, environmental pollution and hobbies, occupational exposure and, partly, fish consumption. The speciation of mercury (Hg0, Hg++, methylmercury and ethylmercury) in biological media, should provide additional and important information in evaluating mercury toxicity. CONCLUSION: It was stressed that the appropriate choice of exposure indicators has to take account of the different variability factors and the characteristics of the toxic kinetics of mercury. The results of biological monitoring must be compared with references values, which are generally in the order of several micrograms/g creatinine, and limit values such as ACGIH BEI (U-Hg 35 micrograms/g creatinine and B-Hg 15 micrograms/l) or the DFG BAT (U-Hg 100 micrograms/l and B-Hg 25 micrograms/l).     

A nine year follow up study of renal effects in workers exposed to cadmium in a zinc ore refinery.

Renal changes with time have been studied in 14 workers engaged in the production of cadmium (Cd) in a zinc ore refinery. These workers were examined once a year in the period 1980 to 1985 and 13 of them also in 1989. Four of the workers (group A) had been employed in an old Cd plant before 1973 and had received higher exposures to Cd than the other workers (group B). Average urinary Cd concentrations over the whole study period in workers of group A ranged from 6.9 to 9.2 micrograms/g creatinine (median 8.4 micrograms/g) and in workers of group B from 0.64 to 7.1 micrograms/g creatinine (median 1.9 micrograms/g). Renal effects were assessed by the determination of urinary N-acetyl-beta-D-glucosaminidase (NAG), beta 2-microglobulin (beta 2-M), retinol binding protein, albumin, total protein, and serum creatinine concentrations and activity. Urinary beta 2-M concentrations in three of four workers of group A were close to or marginally above the upper normal limit during the study period. The beta 2-microglobinuria was not, however, progressive. No values outside normal limits were detected for any of the other renal tests in workers of groups A and B, related to exposure to Cd. Dose-response relations showed that urinary Cd correlated significantly with urinary NAG activity and total protein and beta 2-M. The earliest change induced by Cd was seen for urinary NAG activity within normal limits of NAG excretion. The regression lines were similar in the surveys between 1981 and 1989, indicative of no progression to higher values for any of the renal tests. The current biological exposure index (BEI) of 10 micrograms/g creatinine for workers exposed to Cd, set by the American Conference of Governmental Industrial Hygienists (ACGIH), therefore seems justified, although the safety margin is small. The World Health Organisation recommended limit and ACGIH (1992-3) proposed limit of 5 micrograms/g creatinine would provide a much larger safety margin, and could be regarded as an action point for increased health surveillance.     

Enzymuria in a population living near a cadmium battery plant.

OBJECTIVES--To study the body burden of cadmium and signs of tubular dysfunction in a rural population living near a closed nickel cadmium battery plant. METHODS--Cadmium and N-acetyl-beta-glucosaminidase (NAG) in urine were measured in 72 subjects who lived close to the plant. RESULTS--Residents living close to the plant had higher median urinary cadmium concentrations than those living farther away (1.01 v 0.46 nmol/mmol creatinine) and than a control group (0.2 nmol/mmol creatinine). There was a significant correlation between urinary cadmium and the excretion of NAG in urine as well as signs of tubular dysfunction in residents who excreted urinary cadmium above 0.5 nmol/mmol creatinine. CONCLUSION--Tubular dysfunction may appear in environmentally exposed subjects at lower cadmium body burdens than previously anticipated.     

Renal and immunologic markers for chloralkali workers with low exposure to mercury vapor

OBJECTIVES: The aim of this study was to investigate renal function and immunologic markers among chloralkali workers with long-term low exposure to mercury vapor. METHODS: Forty-seven currently exposed workers were compared with reference workers matched for age in a cross-sectional design. RESULTS: The mean urinary mercury concentration was 5.9 (range 1.1-16.8) nmol/mmol creatinine (Cr) for the exposed workers and 1.3 (range 0.2-5.0) nmol/mmol Cr for the referents. The chloralkali workers had been exposed for an average of 13.3 (range 2.8-34.5) years. The activity of N-acetyl-beta-D-glucosaminidase in urine (U-NAG) was higher in the exposed workers (mean 0.18 U/mmol Cr versus 0.14 U/mmol Cr, P=0.02). Associations between current urinary mercury, cumulative urinary mercury, and cumulative urinary mercury per year (intensity) and U-NAG, autoantibodies to myeloperoxidase (anti-MPO) and proteinase 3 in serum, respectively, were observed. The activity of U-NAG and anti-MPO was increased in the workers with the highest exposure, as assessed by their mean intensity of exposure. The highest activity of U-NAG was observed in the exposed workers with the lower concentrations of selenium in whole blood. CONCLUSIONS: The study indicates an effect of exposure on the kidney proximale tubule cells, possibly modified by individual selenium status, and an effect mediated by neutrophil granulocytes.     

Renal effects of low doses of mercury

OBJECTIVES: The present study was aimed at investigating early markers of renal damage and dysfunction in subjects exposed to low doses of mercury from different sources. Different groups of subjects were examined with urinary Hg excretion (HgU) ranging from 0.1 to 35.0 micrograms/g creatinine: 122 occupationally exposed workers, 22 subjects living in a non-polluted area, but consuming large amounts of tuna and sword fish, and 197 controls. METHODS: Several markers of renal changes were measured in urine (albumin, fibronectin, beta 2-microglobulin, retinol-binding protein, tubular antigens, N-acetyl-beta-D-glucosaminidase activity) and serum (beta 2-microglobulin and cystatin C). Serum autoantibodies towards collagen, laminin and tubular antigens were assessed in subjects with abnormal renal markers. The role of glutathione-S-tranferases GSTT1 and GSTM1 polymorphisms in the inter-individual variability of biological response to Hg was also investigated. RESULTS: Renal markers were not correlated with HgU. None of such markers differed significantly between exposed workers and controls, except for urinary beta 2-microglobulin, which was decreased in Hg-exposed workers (GM = 55.8 vs 86.6 micrograms/g creatinine), in the absence of any changes in serum concentration. Subjects usually eating tuna and sword fish showed an increased urinary excretion of beta 2-microglobulin, albumin and fibronectin. Serum titres of auto-antibodies did not differ between the groups. Neither in controls nor in exposed workers were the observed differences modified by the GSTM1 and GSTT1 genotypes. CONCLUSION: The present study did not provide evidence of any changes in kidney integrity and function in subjects exposed to very low levels of inorganic Hg resulting in urinary Hg lower than 35 micrograms/g creatinine. Nor did we obtain evidence of Hg-induced autoimmunity towards kidney components. The potential modifying role of GST polymorphisms could not be clarified in the absence of effects associated with exposure to the risk factor, i.e., to inorganic Hg. Preliminary data suggesting nephrotoxic effects of organic Hg from a diet rich in large fish resulting in increased levels of both blood and urinary Hg--which however did not exceed 20 micrograms/g creatinine--deserves further investigation.