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Occupational and environmental lead exposure has been associated with significant impairment in renal function. The authors studied the cross-sectional relation between creatinine clearance and blood lead concentration in a population of 744 men participating in the Normative Aging Study of the Department of Veterans Affairs between July 1988 and April 1991. These men, aged 43-90 years, were recruited from communities in the Greater Boston, Massachusetts, area and were selected without regard to lead exposure. The mean values for blood lead concentration and creatinine clearance rate were 8.1 micrograms/dl (standard deviation, 3.9 micrograms/dl) and 88.2 ml/minute (standard deviation, 22.0 ml/minute), respectively. Independent relations of creatinine clearance to blood lead were assessed by multivariate linear regression analysis, with adjustment for various potential confounders. In multivariate linear regression models, the rate of creatinine clearance was significantly and negatively associated with increasing levels of blood lead, even after adjustment for age, body mass index, and use of diuretic and analgesic medications (the beta-coefficient for ln blood lead measured in microgram[microgram/dl]-1 was -0.030; standard error = 0.014, p = 0.037). A rise in ln blood lead of 10.0 micrograms/dl was associated with a decrease in the ln creatinine clearance rate of 10.4 ml/minute. These results support the hypothesis that exposure to low-level environmental lead correlates with a significant decrement in renal function.

Levels of lead in bone serve as a dosimeter for cumulative exposure to lead; moreover, lead in bone may serve as an internal source of circulating lead many years after environmental exposure has ceased. The authors measured lead in blood and used a K-x-ray fluorescence instrument to measure lead in the tibia (cortical) and patella (trabecular) bones in a cross-sectional survey of 719 middle-aged to elderly male participants in the Normative Aging Study who were without unusual occupational exposures to lead and who were healthy when enrolled in 1962-1965. Blood lead levels ranged from < 1 to 27.9 micrograms/dl, with a geometric mean of 5.7 micrograms/dl. Tibia and patella lead level ranges (geometric means) were < 1-51 (20.8) micrograms/g and 3-77 (29.8) micrograms/g, respectively. In backwards elimination multivariate regression models that considered age, race, education, retirement status, measures of both current and cumulative smoking, and alcohol consumption, the factors that remained significantly related to higher levels of both tibia and patella lead were higher age and measures of cumulative smoking, and lower levels of education. In the final model predicting blood lead that began with these same covariates and also included tibia and patella lead, the factor that accounted for the dominant portion of the variance in blood lead was patella lead. After adjustment for measurement error, a rise in patella lead from the median of the lowest to the median of the highest quintiles (13-56 micrograms/g) corresponded to a rise in blood lead of 4.3 micrograms/dl. The authors conclude that bone lead levels are substantial and comprise the major source of circulating lead in these men.