Cadmium, NAG activity, and beta 2-microglobulin in the urine of cadmium pigment workers.

Cadmium (Cd), N-acetyl-beta-D-glucosaminidase (NAG) activity, beta 2-microglobulin (BMG), and creatinine (cr) in urine were measured during April and September 1986 in workers exposed to cadmium pigment dust (maximum exposure 3.0 micrograms/m3/8 h for respirable dust). In April and September urinary Cd ranged from 0.2 to 9.5 and from 0.5 to 7.0 micrograms/g cr with a geometric mean of 0.7 and 1.2 micrograms/g cr, respectively. The correlation coefficient between Cd and NAG was 0.261 (n = 61) in April and 0.389 (n = 50) in September. The correlation coefficient between Cd and BMG was 0.241 (n = 63) in April and 0.115 (n = 50) in September. It appears that urinary Cd concentrations have a closer relation with urinary NAG than urinary BMG, even when urinary Cd concentrations are less than 10 micrograms/g cr. It is concluded that NAG is a more sensitive indicator of Cd absorption than BMG even at urinary Cd concentrations of less than 10 micrograms/g cr.     

Cadmium, NAG activity, and beta 2-microglobulin in the urine of cadmium pigment workers

Cadmium (Cd), N-acetyl-beta-D-glucosaminidase (NAG) activity, beta 2-microglobulin (BMG), and creatinine (cr) in urine were measured during April and September 1986 in workers exposed to cadmium pigment dust (maximum exposure 3.0 micrograms/m3/8 h for respirable dust). In April and September urinary Cd ranged from 0.2 to 9.5 and from 0.5 to 7.0 micrograms/g cr with a geometric mean of 0.7 and 1.2 micrograms/g cr, respectively. The correlation coefficient between Cd and NAG was 0.261 (n = 61) in April and 0.389 (n = 50) in September. The correlation coefficient between Cd and BMG was 0.241 (n = 63) in April and 0.115 (n = 50) in September. It appears that urinary Cd concentrations have a closer relation with urinary NAG than urinary BMG, even when urinary Cd concentrations are less than 10 micrograms/g cr. It is concluded that NAG is a more sensitive indicator of Cd absorption than BMG even at urinary Cd concentrations of less than 10 micrograms/g cr.     

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.     

Significance of the excretion of urinary indicator proteins for a low level of occupational exposure to cadmium

Urinary cadmium (Cd), N-acetyl-beta-D-glucosaminidase (NAG), metallothionein (MT), beta 2-microglobulin (BMG), and blood cadmium were determined in 79 workers who had been employed at a Cd pigment factory in Japan. The workers who had been dealing with Cd pigment manufacturing processes were estimated to be exposed to cadmium pigment dust at a maximum concentration of 3.0 micrograms/m3/8 h for about 20 years. The urinary Cd level ranged from 0.2 to 9.7 micrograms/g creatinine with a geometric mean of 1.02 micrograms/g creatinine. Pearson's correlation coefficients between logarithm of urinary Cd and that of NAG, MT, and BMG in urine were 0.45, 0.62, and 0.05, respectively. The correlation coefficients between blood Cd and urinary NAG, MT, and BMG were 0.21, 0.40, and -0.074, respectively. When partial correlation coefficients were calculated to exclude the contribution of age factor, urinary Cd turned out to be significantly correlated with urinary MT (r = 0.55) and NAG (r = 0.52). The present results indicate that urinary Cd is more closely associated with urinary MT and NAG than with BMG, and suggest that MT and NAG could be good indicators of Cd absorption in a Cd-exposed population whose mean urinary Cd level is relatively low, or less than 10 micrograms/g creatinine.     

Assessment of urinary protein 1 and transferrin as early markers of cadmium nephrotoxicity.

Transferrin and protein 1, a sex linked alpha 2-microprotein, were assayed in urine from 58 workers exposed to cadmium (Cd) in a non-ferrous smelter and from 58 age matched referents. These two new markers of nephrotoxicity were compared with urinary beta 2-microglobulin (beta 2-m), retinol binding protein (RBP), albumin, and beta-N-acetyl-glucosaminidase (NAG). The response of protein 1 to Cd tubulotoxicity was similar to that of beta 2-m, RBP, and NAG. In Cd workers, protein 1 had a correlation with urinary Cd (r = 0.56) similar to beta 2-m (r = 0.48), RBP (r = 0.58), and NAG (r = 0.49). Values of these three low molecular weight proteins and of NAG were increased only in workers with urinary Cd higher than 10 micrograms/g creatinine. Urinary transferrin and albumin were similarly affected by exposure to Cd. Their response, however, was clearly more sensitive than that of low molecular weight proteins. Prevalences of positive values of these two high molecular weight proteins were not only higher but also tended to rise at lower concentrations of Cd in urine or blood. This finding suggests that in some subjects subtle defects in glomerular barrier function may precede the onset of proximal tubular impairment after chronic exposure to Cd. It remains to be assessed whether these subjects are more at risk of developing renal insufficiency.     

Assessment of urinary protein 1 and transferrin as early markers of cadmium nephrotoxicity

Transferrin and protein 1, a sex linked alpha 2-microprotein, were assayed in urine from 58 workers exposed to cadmium (Cd) in a non-ferrous smelter and from 58 age matched referents. These two new markers of nephrotoxicity were compared with urinary beta 2-microglobulin (beta 2-m), retinol binding protein (RBP), albumin, and beta-N-acetyl-glucosaminidase (NAG). The response of protein 1 to Cd tubulotoxicity was similar to that of beta 2-m, RBP, and NAG. In Cd workers, protein 1 had a correlation with urinary Cd (r = 0.56) similar to beta 2-m (r = 0.48), RBP (r = 0.58), and NAG (r = 0.49). Values of these three low molecular weight proteins and of NAG were increased only in workers with urinary Cd higher than 10 micrograms/g creatinine. Urinary transferrin and albumin were similarly affected by exposure to Cd. Their response, however, was clearly more sensitive than that of low molecular weight proteins. Prevalences of positive values of these two high molecular weight proteins were not only higher but also tended to rise at lower concentrations of Cd in urine or blood. This finding suggests that in some subjects subtle defects in glomerular barrier function may precede the onset of proximal tubular impairment after chronic exposure to Cd. It remains to be assessed whether these subjects are more at risk of developing renal insufficiency.     

Urinary neutral endopeptidase in workers exposed to cadmium: interaction with cigarette smoking.

OBJECTIVES: Structural impairment of the renal proximal tubular epithelium induced by cadmium (Cd) was investigated by measuring the concentration of neutral endopeptidase 24.11 (NEP), an ectoenzyme of the apical brush border, in the urine of 106 male workers employed in a Cd smelter (among whom 52 were occupationally exposed to Cd), and by comparing it with other tubular markers (low molecular weight proteins, lysosomal enzymes). METHODS: NEP (EC 3.4.24.11), beta-N-acetyl-glucosaminidase (NAG) (EC 3.2.1.30), and NAG-B isoenzyme activities were measured by fluorimetric assays, whereas the concentrations of retinol binding protein (RBP), beta 2-microglobulin (beta 2M), and Clara cell protein (CC16) were measured by automated latex agglutination techniques. RESULTS: An increased urinary excretion of NEP as well as microproteins was found only in subjects excreting more than 5 micrograms Cd/g creatinine. In this group, NEP concentrations were significantly higher in the subjects who smoked. This significant interaction could not be found for any other marker tested. CONCLUSIONS: The data suggest that NEP enzymuria is high even at low exposures to Cd (with a threshold of urinary cadmium excretion (U-Cd) at 5 micrograms/g creatinine), indicating early structural alterations. Moreover, its particular sensitivity to smoking could be useful in the detection of new population clusters potentially more susceptible to development of nephrotoxic insult.     

Markers of early renal changes induced by industrial pollutants. III. Application to workers exposed to cadmium.

Cadmium (Cd) was the third heavy metal investigated in the European collaborative research project on the development and validation of new markers of nephrotoxicity. Fifty workers exposed to Cd and 50 control workers were examined. After application of selection criteria 37 workers (mean age 43) exposed to Cd for an average of 11.3 years; and 43 age matched referents were retained for final analysis. The average concentrations of Cd in blood (Cd-B) and urine (Cd-U) of exposed workers were 5.5 micrograms Cd/l and 5.4 micrograms Cd/g creatinine respectively. By contrast with lead and mercury, Cd had a broad spectrum of effects on the kidney, producing significant alterations in amounts of almost all potential indicators of nephrotoxicity that were measured in urine--namely, low and high molecular weight proteins, kidney derived antigens or enzymes, prostanoids, and various other biochemical indices such as glycosaminoglycans and sialic acid. An increase in beta 2-microglobulin and a decrease of sialic acid concentration were found in serum. Dose-effect/response relations could be established between most of these markers and Cd-U or Cd-B. The thresholds of Cd-U associated with a significantly higher probability of change in these indicators were estimated by logistic regression analysis. Three main groups of thresholds could be identified: one around 2 micrograms Cd/g creatinine mainly associated with biochemical alterations, a second around 4 micrograms Cd/g creatinine for high molecular weight proteins and some tubular antigens or enzymes, and a third one around 10 micrograms Cd/g creatinine for low molecular weight proteins and other indicators. The recent recommendation by the American Conference of Governmental Industrial Hygienists (ACGIH) of 5 micrograms Cd/g creatinine in urine as the biological exposure limit for occupational exposure to Cd appears thus justified, although for most of the effects occurring around this threshold the link with the subsequent development of overt Cd nephropathy is not established. In that respect, the very early interference with production of some prostanoids (threshold 2 micrograms Cd/g creatinine) deserves further investigation; although this effect might contribute to protect the filtration capacity of the kidneys, it might also play a part in the toxicity of Cd on bone.     

Association between NAG-B and cadmium in urine with no evidence of a threshold.

OBJECTIVES--To explore the significance of the increase in urinary excretion of the lysosomal enzyme beta-N-acetylglucosaminidase (NAG) at low exposures to cadmium (Cd) that is frequently found in the absence of any other sign of renal dysfunction. METHODS--The activity was measured of the two main isoenzymes of NAG (NAG-A secreted by exocytosis and NAG-B released with cell membranes) in the urine of 49 male workers employed in a Cd smelter and of 20 age matched controls. RESULTS--An increased urinary excretion of low molecular weight proteins was noted only in subjects who excreted > 10 micrograms Cd/g creatinine. The urinary activity of NAG-B showed a dose related increase that was already significant in the group excreting 0.5-2 micrograms Cd/g creatinine. In multiple regression analysis the NAG-B activity correlated with the excretion of Cd but not with that of lead or mercury. The NAG-A activity was by contrast unaffected by exposure to Cd but correlated with the urinary excretion of lead and copper. CONCLUSIONS--As NAG-B is considered to be the lesional form of NAG, the existence of a specific association between this enzyme and urinary Cd excretion with no detectable threshold suggests that this metal produces cellular alterations at exposures commonly found in the general population.     

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).     

Significance of the excretion of urinary indicator proteins for a low level of occupational exposure to cadmium

Summary Urinary cadmium (Cd), N-acetyl-β-D-glucosaminidase (NAG), metallothionein (MT), β₂-microglobulin (BMG), and blood cadmium were determined in 79 workers who had been employed at a Cd pigment factory in Japan. The workers who had been dealing with Cd pigment manufacturing processes were estimated to be exposed to cadmium pigment dust at a maximum concentration of 3.0 [μg/m³/8 h for about 20 years. The urinary Cd level ranged from 0.2 to 9.7 μg/g creatinine with a geometric mean of 1.02 μg/g creatinine. Pearson's correlation coefficients between logarithm of urinary Cd and that of NAG, MT, and BMG in urine were 0.45, 0.62, and 0.05, respectively. The correlation coefficients between blood Cd and urinary NAG, MT, and BMG were 0.21, 0.40, and −0.074, respectively. When partial correlation coefficients were calculated to exclude the contribution of age factor, urinary Cd turned out to be significantly correlated with urinary MT (r = 0.55) and NAG (r = 0.52). The present results indicate that urinary Cd is more closely associated with urinary MT and NAG than with BMG, and suggest that MT and NAG could be good indicators of Cd absorption in a Cd-exposed population whose mean urinary Cd level is relatively low, or less than 10 μg/g creatinine.     

Assessment of the filtration reserve capacity of the kidney in workers exposed to cadmium

It has been assessed whether an internal dose of cadmium (Cd), as reflected by a Cd concentration in urine not yet sufficient to induce a significantly increased urinary excretion of various plasma proteins (microproteinuria defined as beta 2-microglobulin in urine greater than 300 micrograms/g creatinine, or retinol-binding protein in urine greater than 300 micrograms/g creatinine, or albumin in urine greater than 15 mg/g creatinine, or a combination of these), may affect the filtration reserve capacity of the kidney. The last was determined by measuring the difference between the baseline creatinine clearance and the maximal creatinine clearance after an acute oral load of protein (400 g of cooked red meat). In total 215 men were examined of whom eventually 87 Cd exposed workers (concentration of Cd in urine greater than 2 micrograms/g creatinine) from zinc/cadmium smelters and 92 control workers (concentration of Cd in urine less than 2 micrograms/g creatinine, absence of microproteinuria, normal fasting serum creatinine) were retained for data analysis performed separately for workers aged less or more than 50 years. Microproteinuria was present in 20 Cd workers, all older than 50. This study confirmed the previous observation that the age related decline of the baseline glomerular filtration rate (GFR) is accelerated in male workers with Cd induced microproteinuria; the same observation was made for the maximal GFR. It was found, however, that a renal Cd burden that had not yet caused microproteinuria did not impair the filtration reserve capacity of the kidney. This study therefore validates the previous estimate of the threshold effect concentration of Cd in urine (10 micrograms/g creatinine) that is intended to prevent the occurrence of microproteinuria in male Cd workers. It should be kept in mind, however, that because of the likely interference of the healthy worker effect, this conclusion may not be directly extrapolated to the general population.     

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.     

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.     

Assessment of the filtration reserve capacity of the kidney in workers exposed to cadmium.

It has been assessed whether an internal dose of cadmium (Cd), as reflected by a Cd concentration in urine not yet sufficient to induce a significantly increased urinary excretion of various plasma proteins (microproteinuria defined as beta 2-microglobulin in urine greater than 300 micrograms/g creatinine, or retinol-binding protein in urine greater than 300 micrograms/g creatinine, or albumin in urine greater than 15 mg/g creatinine, or a combination of these), may affect the filtration reserve capacity of the kidney. The last was determined by measuring the difference between the baseline creatinine clearance and the maximal creatinine clearance after an acute oral load of protein (400 g of cooked red meat). In total 215 men were examined of whom eventually 87 Cd exposed workers (concentration of Cd in urine greater than 2 micrograms/g creatinine) from zinc/cadmium smelters and 92 control workers (concentration of Cd in urine less than 2 micrograms/g creatinine, absence of microproteinuria, normal fasting serum creatinine) were retained for data analysis performed separately for workers aged less or more than 50 years. Microproteinuria was present in 20 Cd workers, all older than 50. This study confirmed the previous observation that the age related decline of the baseline glomerular filtration rate (GFR) is accelerated in male workers with Cd induced microproteinuria; the same observation was made for the maximal GFR. It was found, however, that a renal Cd burden that had not yet caused microproteinuria did not impair the filtration reserve capacity of the kidney. This study therefore validates the previous estimate of the threshold effect concentration of Cd in urine (10 micrograms/g creatinine) that is intended to prevent the occurrence of microproteinuria in male Cd workers. It should be kept in mind, however, that because of the likely interference of the healthy worker effect, this conclusion may not be directly extrapolated to the general population.     

Potential nephrotoxic effects of exposure to silver

A cross sectional study was conducted on workers engaged in manufacturing precious metal powder. Of the 27 workers, 96% had raised urine silver concentrations (range 0.5-52.0 micrograms/l, mean 11.3 micrograms/l) and 92% had raised blood silver concentrations (range 0.05-6.2 micrograms/100 ml, mean 1.0 microgram/100 ml). Nineteen per cent also had raised urine cadmium concentrations (range 1.9-76.0 micrograms/l, mean 11.8 micrograms/l). Most workers had symptoms of respiratory irritation and nose bleeds were reported in eight (30%) of the 27 workers. Deposition of silver in the cornea of the eye was detected in five of eight (63%) of the long term workers. Although not statistically significant, corneal deposition was associated with complaints of decreased night vision. The urinary enzyme N-acetyl-B-D glucosaminidase (NAG) was significantly raised in four individuals and was correlated with blood silver concentrations and age. In addition, the group's average NAG concentration was significantly higher than that found in a control population. No association between age and urinary NAG was found in the control group. Estimated creatinine clearance was also significantly lower in the group exposed to silver than in the control group. Kidney function appears to have been adversely affected by exposures at work but because of the exposure to cadmium the role of silver in causing the decrement in kidney function could not be definitely determined.     

Potential nephrotoxic effects of exposure to silver.

A cross sectional study was conducted on workers engaged in manufacturing precious metal powder. Of the 27 workers, 96% had raised urine silver concentrations (range 0.5-52.0 micrograms/l, mean 11.3 micrograms/l) and 92% had raised blood silver concentrations (range 0.05-6.2 micrograms/100 ml, mean 1.0 microgram/100 ml). Nineteen per cent also had raised urine cadmium concentrations (range 1.9-76.0 micrograms/l, mean 11.8 micrograms/l). Most workers had symptoms of respiratory irritation and nose bleeds were reported in eight (30%) of the 27 workers. Deposition of silver in the cornea of the eye was detected in five of eight (63%) of the long term workers. Although not statistically significant, corneal deposition was associated with complaints of decreased night vision. The urinary enzyme N-acetyl-B-D glucosaminidase (NAG) was significantly raised in four individuals and was correlated with blood silver concentrations and age. In addition, the group's average NAG concentration was significantly higher than that found in a control population. No association between age and urinary NAG was found in the control group. Estimated creatinine clearance was also significantly lower in the group exposed to silver than in the control group. Kidney function appears to have been adversely affected by exposures at work but because of the exposure to cadmium the role of silver in causing the decrement in kidney function could not be definitely determined.     

Assessment of occupational exposure to cadmium in The Netherlands, 1980-1989.

One thousand five hundred fifty urine samples and 1,295 blood samples, collected from 919 workers, were analyzed for cadmium (Cd). The workers were employed at 16 different types of workplaces. In about 7.5% of the samples, the concentration of Cd exceeded the biological limit values proposed by the Dutch Expert Committee for Occupational Standards. Levels higher than these values were measured in both urine samples and blood samples of workers involved in electrochemical plating, in production of Cd-stabilizers and enamels, and in soldering with silver-cadmium solder. Significantly higher concentrations of beta 2-microglobulin (MG) were found in urine samples with CdU greater than 10 micrograms/g creatinine. Cd levels in urine increased with age.     

铅作业工人肾损伤某些生化指标的变化

目的　探索铅致肾损伤生化指标的变化。方法　观察了某蓄电池厂 10 3名铅作业工人尿总蛋白(TP)、尿β2 微球蛋白 (β2 MG)、尿N 乙酰 β D 氨基葡萄糖苷酶 (NAG)的变化 ,同时分析尿铅含量、接触工龄与三指标的关系。结果　接触组尿TP(5 9 73± 6 84 )mg gCr、尿 β2 MG(12 2 0 1± 1 2 5 ) μg gCr、尿NAG(13 70±1 6 2 )U gCr水平显著高于对照组 ,且随尿铅含量的增高而升高。尿NAG的活性在接触铅 1～ 3年明显高于对照组 ,先于尿TP、尿 β2 MG出现异常。结论　尿NAG活性升高可能反映肾小管细胞损伤。尿NAG活性变化 ,结合尿β2 MG或尿TP的变化 ,可能反映肾受损情况。