We studied whether lead exposure increased the serum lipid peroxide (LPO) level and inhibited blood superoxide dismutase (SOD) activity in workers with occupational exposure to lead and rats injected with lead. We examined the following subjects: (1) manual workers (712 males) from 18 to 59-years-old in steel production with occupational exposure to lead, (2) office workers (155 males) without exposure to lead, (3) rats subcutaneously injected with lead in concentrations of 10 or 20 mg/kg as lead acetate. The nutritional intakes of manual workers and office workers were approximately equal. Serum LPO and high-density lipoprotein cholesterol (HDL-CL) levels in manual workers (LPO: 4.4 +/- 1.9 nmol/ml, HDL-CL: 55.6 +/- 14.2 mg/dl) were significantly higher than those in office workers (LPO: 4.0 +/- 1.4 nmol/ml, HDL-CL: 53.0 +/- 13.9 mg/dl). Serum LPO level in the manual workers increased with an increase of the lead concentration in the blood, while blood SOD activity decreased. Similar phenomena were observed in rats subcutaneously injected with lead acetate. Furthermore, the addition of lead at higher than 20-microM concentrations to non-treated rats liver microsomes increased NADPH-dependent liquid peroxidation, and these lead concentrations inhibited bovine erythrocyte SOD activity in vitro assay system. In conclusion, the present results seem to indicate that the increase of serum LPO level in workers with occupational exposure to lead is due not only to the stimulation of lipid peroxidation, but also to the inhibition of SOD activity by exposure to lead in the manufacturing processes.
The resolution of radiologic and neurologic abnormalities and altered autoantibody titers against neutral glycolipids after immunotherapy suggest that EMRN is caused by an immune-mediated mechanism. These autoantibodies may be useful biomarkers for EMRN.
Abstract:The relationship between airborne concentration of beryllium in the working environment and workers' beryllium lymphocyte transformation test (Be-LTT) values was examined based on data obtained from a four-year survey (1992)(1993)(1994)(1995) conducted at beryllium-copper alloy manufacturing factories. This study showed that the T cells of workers continuously exposed to beryllium of more than 0.01 /Im3 could be activated and that the cell-mediated immune response of workers could be promoted. On the other hand, the Be-LTT of workers exposed to beryllium levels of less than 0.01 pglm3 was shown to be unaffected by beryllium. These findings suggest that beryllium sensitization is not manifested when level of beryllium in working environment are less than 0.01 pglm3. Therefore, in such cases workers do not develop Chronic beryllium disease (CBD). We concluded that the Be-LTT can be applied as a medical indicator to detect the development of CBD.
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