Abstract
BackgroundRecent studies in children have reported associations of urinary cadmium (U-Cd), used as biomarker of Cd body burden, with renal dysfunction, retarded growth and impaired cognitive development in children. Little is known, however, about factors influencing U-Cd in children and likely to act as confounders.MethodsIn a cross-sectional study involving 249 schoolchildren (mean age, 5.72 years; 138 boys), we measured the urine concentrations of cadmium, zinc, lead, albumin, alpha1-microglobulin (A1M), retinol-binding protein, β2-microglobulin and club cell protein (CC16). Determinants of U-Cd expressed per creatinine or adjusted to specific gravity were identified by multiple regression analyses.ResultsGirls and boys had similar median concentrations of U-Cd (0.22 and 0.24 μg/L, 0.33 and 0.35 μg/g creatinine, respectively). When models were run without including creatinine or specific gravity among independent variables, urinary zinc, urinary A1M and age emerged as the strongest predictors of U-Cd expressed per g creatinine or adjusted to SG. When adding creatinine among predictors, urinary creatinine emerged as an additional strong predictor correlating negatively with U-Cd per g creatinine. This strong residual influence of diuresis, not seen when adding specific gravity among predictors, linked U-Cd to U-A1M or U-CC16 through secondary associations mimicking those induced by Cd nephrotoxity.ConclusionsIn young children U-Cd largely varies with diuresis, zinc metabolism and urinary A1M. These physiological determinants, unrelated to Cd body burden, may confound the child renal and developmental outcomes associated with low-level U-Cd.
Highlights
Recent studies in children have reported associations of urinary cadmium (U-Cd), used as biomarker of Cd body burden, with renal dysfunction, retarded growth and impaired cognitive development in children
The urinary concentrations of β2microglobulin (U-β2m), alpha1-microglobulin (U-A1M), club cell protein (U-CC16), retinol-binding protein (URBP) and albumin (U-Alb) were determined by automated latex immunoassays using Dakopatts antibodies and standards based on commercially available proteins or on proteins purified in our laboratory [20,21,22,23]
Associations of alpha1-microglobulin in urine (U-A1M), club cell protein in urine (U-CC16) and U-β2m with creatinine in urine (U-Creat), initially positive, turned negative when expressing the concentrations per g creatinine
Summary
Recent studies in children have reported associations of urinary cadmium (U-Cd), used as biomarker of Cd body burden, with renal dysfunction, retarded growth and impaired cognitive development in children. Wang et al Environmental Health (2017) 16:99 dietary intakes or occupational exposures to Cd. The vast majority of epidemiological studies relied on this concept when implicating low-level Cd exposure as a risk factor for bone, cardiovascular and other degenerative diseases [1]. The vast majority of epidemiological studies relied on this concept when implicating low-level Cd exposure as a risk factor for bone, cardiovascular and other degenerative diseases [1] In these studies, the use of U-Cd as indicator of Cd body burden is an argument for excluding the possibility of reverse causation since in most cases the studied outcomes (e.g. renal or developmental effects) are unlikely to increase the body burden of the heavy metal. Several studies among children with low dietary exposure to Cd have associated an increase of U-Cd with renal dysfunction (decreased glomerular filtration rate and increased proteinuria), retarded growth and impaired cognitive development (learning disability, special education utilization, cognitive delays) [5,6,7,8,9,10]
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