Although nephrotoxicity is common following exposure to lead, the dose-response relationship in adults with occupational exposure is not well understood because information is lacking on early nephrotoxic effects. By the time serum urea nitrogen and creatinine levels are elevated, renal damage may be advanced and not fully reversible. Detailed investigations of renal glomerular and tubular function were performed in six adults with occupational exposure to lead. In all patients, the serum creatinine and urea nitrogen concentrations were within the normal range. GFR was decreased in all but two. Glucose reabsorptive capacity (TmG) was decreased in all, and this decrease was disproportionately greater than expected from the reduced GFR in all but one. Normal values for renal plasma flow (RFP) were observed in four of the six, and for rho-aminohippurate (PAH) secretory capacity (TmPAh) in all but one. Bicarbonate reabsorptive capacity (TmHCO3) and urinary excretion of beta2-microglobulin were normal in all. Routine clinical laboratory tests are insensitive for the detection of early renal effects of heavy metal exposure. Measurements of renal tubular reabsorptive capacity for glucose appears to be a sensitive method for the early detection of renal effect of lead.
Air lead and blood lead data, recorded over a period of 3 years for 972 employees at an automobile battery factory as part of a lead control program, were summarized and statistically analyzed. The air lead values were measured by mobile area samplers for approximately 2 years and then by personal samplers for approximately 1 year. Blood lead analyses were usually performed once a month for most of the workers. The trend in air lead levels was significantly upward in the 1st year and significantly downward in the 2nd year while the trend in blood lead levels was significantly downward in the 1st year and in the 3rd year. There were no other significant trends. To assess the relationship between air lead and blood lead, data were used whenever an air lead obtained by personal sampler was followed within 1 month by a blood lead on the same worker. The variables age, job tenure, and department identity were included in an analysis of covariance. Only air lead and departments were significant, accounting for 9% and 13% of the variance in blood lead, respectively. From these data 95% confidence limits were calculated for predicting blood leads from given air leads for an individual worker. These were 30-68 micrograms/100 ml at 200 micrograms/m3, 25-62 micrograms/100 ml at 100 micrograms/m3, and 22-60 micrograms/100 ml at 50 micrograms/m3.
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