Co-exposure to lead increases the renal response to low levels of cadmium in metallurgy workers

R Hambach,D Lison,P.C D’Haese,J Weyler,E De Graef,A De Schryver,L.V Lamberts,M Van Sprundel

doi:10.1016/j.toxlet.2013.06.218

R Hambach, D Lison + Show 6 more

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https://doi.org/10.1016/j.toxlet.2013.06.218

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Abstract

PurposeResearch on the effect of co-exposure to Cd and Pb on the kidney is scarce. The objective of the present study was to assess the effect of co-exposure to these metals on biomarkers of early renal effect. MethodsCd in blood (Cd-B), Cd in urine (Cd-U), Pb in blood (Pb-B) and urinary renal biomarkers, i.e., microalbumin (μ-Alb), beta-2-microglobulin (β2-MG), retinol binding protein (RBP), N-acetyl-β-d-glucosaminidase (NAG), intestinal alkaline phosphatase (IAP) were measured in 122 metallurgic refinery workers examined in a cross-sectional survey. Results and conclusionsThe median Cd-B, Cd-U, Pb-B were: 0.8μg/l (IQR=0.5, 1.2), 0.5μg/g creatinine (IQR=0.3, 0.8) and 158.5μg/l (IQR=111.0, 219.3), respectively. The impact of Cd-B on the urinary excretion of NAG and IAP was only evident among workers with Pb-B concentrations ≥75th percentile. The association between Cd-U and the renal markers NAG and RBP was also evidenced when Pb-B ≥75th percentile. No statistically significant interaction terms were observed for the associations between Cd-B or Cd-U and the other renal markers under study (i.e., μ-Alb and β2-MG). Our findings indicate that Pb increases the impact of Cd exposure on early renal biomarkers.

Highlights

Cadmium (Cd) and lead (Pb) are widespread occupational and environmental toxicants
Cd in blood (Cd-B), Cd in urine (Cd-U), Pb in blood (Pb-B) and urinary renal biomarkers, i.e., microalbumin (␮-Alb), beta-2-microglobulin (␤2-MG), retinol binding protein (RBP), N-acetyl-␤-dglucosaminidase (NAG), intestinal alkaline phosphatase (IAP) were measured in 122 metallurgic refinery workers examined in a cross-sectional survey
Our findings indicate that Pb increases the impact of Cd exposure on early renal biomarkers

Summary

Introduction

Inhalation and ingestion are the two main routes of exposure to Cd and Pb (Johri et al, 2010), inhalation being. The Cd-MT complex is released back into the circulation This complex of low molecular weight is freely filtered through the glomerulus and reabsorbed by the proximal tubule (PT) (Johri et al, 2010; Nordberg, 2009; Sabath and RoblesOsorio, 2012). Cd up-regulates the MT production in the liver and kidney to limit the toxicity of unbound Cd. The kidney is the primary target of toxicity with respect to chronic exposure to Cd (Johri et al, 2010). When the renal capacity to produce MT is overwhelmed, renal tubular dysfunction may occur, as reflected by an increased urinary excretion of low-molecular-weight (LMW) proteins e.g., beta-2-microglobulin (␤2-MG) and retinol binding protein (RBP), and renal proximal tubular damage characterized by an excretion

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Conclusion