Blood Lead Level and Kidney Function in US Adolescents

Abstract

Background Chronic, high-level lead exposure is a known risk factor for kidney disease. The effect of current low-level environmental lead exposure is less well known, particularly among children, a population generally free from kidney disease risk factors such as hypertension and diabetes mellitus. Therefore, in this study, we investigated the association between lead exposure and kidney function in a representative sample of US adolescents. Methods Participants included 769 adolescents aged 12 to 20 years for whom whole blood lead and serum cystatin C were measured in the Third National Health and Nutrition Examination Survey, conducted from 1988–1994. The association between blood lead level and level of kidney function (glomerular filtration rate [GFR]), determined by cystatin C–based and creatinine-based estimating equations, was examined. Results Median whole blood lead level was 1.5 μg/dL (to convert to micromoles per liter, multiply by 0.0483), and median cystatin C–estimated GFR was 112.9 mL/min/1.73 m2. Participants with lead levels in the highest quartile (≥3.0 μg/dL) had 6.6 mL/min/1.73 m2–lower estimated GFR (95% confidence interval, −0.7 to −12.6 mL/min/1.73 m2) compared with those in the first quartile (<1 μg/dL). A doubling of blood lead level was associated with a 2.9 mL/min/1.73 m2–lower estimated GFR (95% confidence interval, −0.7 to −5.0 mL/min/1.73 m2). Lead levels were also associated with lower creatinine-based estimated GFR levels, but the association was weaker than with cystatin C–based GFR and not statistically significant. Conclusions Higher blood lead levels in a range below the current Centers for Disease Control and Prevention–designated level of concern (10 μg/dL) were associated with lower estimated GFRs in a representative sample of US adolescents. This finding contributes to the increasing epidemiologic evidence indicating an adverse effect of low-level environmental lead exposure.

The Protective Effect of Baicalin Against Lead-Induced Renal Oxidative Damage in Mice

“…However, excessive exposure to it could cause a variety of toxic effects, among which is its adverse influence on the kidney. An increasing number of studies have also indicated the unexpected effects and pathogenic mechanisms of Pb on renal function [3][4][5]. Among the various pathogenic mechanisms of renal injury, oxidative stress influences glomerular structure and function mainly depending upon the effect of reactive oxygen species (ROS) on mesangial and endothelial cells [6].…”

Toxic environmental exposures and kidney health in children

“…Multiple cross-sectional studies in adults have demonstrated a significant positive association between blood lead level and serum creatinine [62-64], as well as increased all-cause and cardiovascular mortality [65]. An analysis of 769 adolescents participating in the 1988–1994 NHANES with median blood lead and cystatin C-based eGFR levels of 1.5 μg/dL and 112.9 mL/ min/1.73 m 2 , respectively, identified a statistically significant, negative association between blood lead level and kidney function [66]. In fully adjusted models, cystatin C-based eGFR was lower (−6.6 mL/min/1.73 m 2 ; 95 % CI −0.7 to −12.6) in children with lead levels in the highest quartile (≥3.0 μg/dL) compared with those in the lowest quartile (<1 μg/dL).…”

Basics of Clinical Investigation

“…This data lends itself well to cross-sectional studies. The association between lead levels in children and estimated glomerular filtration rate (GFR) was examined among 769 children who participated in the survey from 1988 to 1994 [3]. As can be observed in Fig.…”

“…Data points for the scatterplot represent adjusted blood lead and estimated GFR values. The horizontal axis is in the log scale (From Fadrowski and Navas-Acien [3], figure) simultaneously, and the investigator must infer cause and effect relationships because the temporal sequence cannot be established. In a case-control design, an attempt to establish a temporal relationship between the outcome and exposure is made by starting with a population of persons with and without the outcome and then working backward to examine suspected exposures.…”