Background: The kidneys are one of the main target organs for elemental mercury (Hg(0)). The influence of Hg(0) on kidneys has been extensively studied but the long-term effects on this organ have not yet been determined with certainty. The basic aim of this research was to study the effects of a long-term exposure to Hg(0) vapours on the renal function in miners in the post-exposure period.
Methods: The population studied comprised 53 miners (33 active and 20 retired) from the Idrija Mercury Mine as the exposed miners group and 53 unexposed workers as the control group. On the basis of mine exposure records (air and biological monitoring), the environmental and biological indicators of the past exposure to Hg(0) were calculated for each miner. Kidney function was determined in both groups, i.e. in the exposed miners as well as in the controls. Glomerular kidney function was evaluated by a quantitative analysis of albumin and IgG in urine. Tubular kidney function, however, was determined by a quantitative analysis of alpha(1)-microglobulin in urine and by the enzymatic activity of N-acetyl-beta-d-glucosaminidase (NAG).
Results: The mean exposure time in miners was 15 years. The total number of cycles of exposure ranged from 13 to 119. The mean annual time-weighted exposure was 0.29 mg m(-3) and the mean integrated exposure intensity (IEI) was 1413 mg m(-3)-h. Throughout the period of exposure the average urine mercury concentration in miners was 68.24 microg l(-1) and the average sum of peak urine mercury concentrations was 3901 microg l(-1). Albumin, IgG and alpha(1)-microglobulin in urine were significantly elevated in the exposed miners compared with the unexposed controls (t = 2.17, P = 0.03; t = 2.81, P < 0.01; and t = 2.07, P = 0.04). No significant differences were found in the urine NAG activity when the exposed miners and the unexposed workers were compared. Among the indicators of renal function only alpha(1)-microglobulin in the urine correlated significantly with the IEI (r = 0.73; P <or= 0.01) and with the sum of peak mercury urine concentrations (r = 0.67; P <or= 0.01) in the group of miners who still worked, while no significant correlations were found between these parameters in the group of the retired miners.
Conclusion: The results of the differences in albumin, IgG and alpha(1)-microglobulin concentrations in urine between the exposed miners and unexposed controls suggest that a long-term occupational exposure to Hg(0) could cause renal dysfunction. A high correlation between alpha(1)-microglobulin in urine and the IEI as well as between alpha(1)-microglobulin in urine and the sum of peak urine mercury concentrations in the group of active but no longer exposed miners indicates that a long-term occupational exposure to Hg(0) may cause a non-permanent tubular dysfunction.