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Cadmium(Cd)and lead(Pb)are widespread occupational and environmental toxicants.High exposure to Cd is known to cause renal tubular dysfunction reflected by an increased urinary excretion of low-molecular-weight(LMW)proteins e.g.,beta-2-microglobulin(β2-MG)and retinol binding protein(RBP),and renal proximal tubular damage characterized by an excretion of urinary enzymes e.g.,N-acetyl-β-D-glucosaminidase(NAG)and urinary intestinal alkaline phosphatase(IAP).Pb exposure affects the glomerular function(e.g.,renal hyperfiltration).Yet,renal tubular effects are also reported by several authors.High exposure to Cd and Pb rarely occurs in most industrialized countries,but chronic combined low exposure to these metals are still a major public health issue.Cd and Pb exposure are reported in a number of industries(e.g.,construction,manufacturing of jewels,electroplating,welding,automobile industry,production of pigments,metal recycling industry).Recent research suggests adverse renal effects in adults at low level of Cd and Pb exposure i.e.,Cd in urine(Cd-U)< 2.0 μg/g creatinine and Pb in blood(Pb-B)< 10 μg/l.Several epidemiological studies have underlined that isolated environmental or occupational exposure to Cd rarely occurs and is often associated with Pb exposure.Research on the effect of combined exposure to Cd and Pb on the kidney in humans however,is scarce.As Cd and Pb can interact with each other in a complex way co-exposure to Cd and Pb may induce additive or synergistic interactions or even new effects that are not described in single element exposure.During this lecture 1)indicators of low to moderate Cd and Pb exposure 2)assessment of early biomarkers of subclinical renal effect(i.e.,β2-MG,μ-Alb,RBP,NAG,IAP)and,3)the effect of co-exposure to Pb and Cd on these biomarkers will be dealt with.