ArticlesRenal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study
Introduction
The renal toxicity of cadmium has been documented in highly exposed populations in occupational settings.1 Environmental pollution by cadmium may also induce a subclinical renal response with low-molecular-weight proteinuria and calciuria.1 However, whereas there is good evidence indicating that occupational exposure to cadmium can lead to irreversible tubular effects and possibly glomerular dysfunction, the clinical relevance and the course of the renal effects documented in environmentally exposed populations remain uncertain. On the one hand, a few longitudinal investigations suggested that the renal effects induced by environmental cadmium exposure were not only irreversible but also progressive even after cessation of exposure and some cases of chronic renal failure or uraemia associated with environmental cadmium exposure have been reported.2, 3, 4, 5 On the other hand, studies6, 7, 8 on mortality due to renal disease in populations environmentally exposed to cadmium have provided controversial results. A possible explanation for these inconsistencies may be that the results of some studies have been distorted by biases and confounding factors, which may have caused an overestimation of risk of severe kidney damage induced by environmental cadmium exposure.
In a previous study between 1985 and 1989 we surveyed populations environmentally exposed to cadmium in Belgium (Cadmibel9). That study showed an association between cadmium exposure and increased prevalence of abnormal results of kidney function tests (above the 95th centile in the control group). In particular, the urinary excretion of calcium, β2-microglobulin, retinol-binding protein, and N-acetyl-β-D-glucosaminidase (NAG) was significantly associated with the cadmium body burden as assessed by the urinary excretion of the metal. There was a 10% probability of values of these variables being higher than normal when cadmium excretion exceeded 2–4 μg/24 h.
The primary purpose of our investigation was to follow the course of the cadmium-induced renal effects ascertained in the most exposed subgroup from the Cadmibel study. A second purpose was to examine, the relation between indicators of renal tubular effects and cadmium body burden and the possible development of glomerular dysfunction.
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Study population
The design of the study has already been described.10 Briefly, the first study took place in four areas defined by urbanisation grade and environmental cadmium pollution level. The study population was recruited to have equal numbers of individuals in six subgroups stratified by sex and age (20–39 years, 40–59 years, 60–79 years) and drawn from a random sample of households. 2327 of 4532 eligible individuals took part. After this first survey (Cadmibel study, 1985–89, baseline values9) the
Results
The median duration of follow-up was 5·2 years (range 4·6–6·1). The characteristics of the individuals who took part in both examinations are presented in table 1. Urinary cadmium excretion and blood cadmium concentrations decreased slightly in both sexes during follow-up. Overall, mean values of renal variables and prevalence of higher than normal values decreased, suggesting reversibility of the effects of cadmium on the kidney. Microalbuminuria (30–300 mg/24 h) was present in 13 (6·5%) men
Discussion
The main finding of this study is that no sign of glomerular dysfunction or progression of cadmiuminduced renal damage was found in this population with environmental exposure to cadmium and followed up over 5 years.
The strengths of this study are the size of the cohort, the random selection of households, quality control over the whole study period, a well-documented exposure assessment (cadmium, lead, copper, zinc, arsenic)12, 18 and the consideration of several confounding factors (table 2).
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