In a cross-sectional population study to assess whether environmental exposure to cadmium is associated with renal dysfunction, 1699 subjects aged 20-80 years were studied as a random sample of four areas of Belgium with varying degrees of cadmium pollution. After standardisation for several possible confounding factors, five variables (urinary excretion of retinol-binding protein, N-acetyl-beta-glucosaminidase, beta 2-microglobulin, aminoacids, and calcium) were significantly associated with the urinary excretion of cadmium (as a marker of cadmium body burden), suggesting the presence of tubular dysfunction. There was a 10% probability of values of these variables being abnormal when cadmium excretion exceeded 2-4 micrograms/24 h. Excretion reached this threshold in 10% of non-smokers. There was also evidence that diabetic patients may be more susceptible to the toxic effect of cadmium on the renal proximal tubule.

In a population study conducted from 1985 to 1989 in Belgium, the authors investigated whether exposure to cadmium is associated with blood pressure elevation and with an increased prevalence of cardiovascular diseases. The participants, aged 20-88 years, constituted a random sample of the households living in two low exposure areas (n = 803) and two high exposure areas (n = 1,283). For each exposure level, a rural and an urban district were selected. The cadmium levels in blood (8.5 vs. 11.0 nmol/liter) and urine (7.2 vs. 8.7 nmol/24 hours) were significantly (p less than 0.001) raised in the two high exposure areas compared with the two low exposure areas (p less than 0.001). Systolic pressure was similar in both rural areas, but in the urban area with high exposure systolic pressure was 5 mmHg (p less than 0.001) higher than in the control town. Diastolic pressure was similar in the four districts and the same was true for the prevalence of hypertension and of other cardiovascular diseases. Adjustment of systolic pressure for blood and urinary cadmium did not remove the difference in systolic pressure between both urban areas, suggesting that it was not related to the cadmium burden on the environment. Further analyses in individual subjects showed that neither blood pressure nor the presence of cardiovascular diseases were significantly and positively correlated with blood and urinary cadmium. Thus, the present population study did not confirm the hypothesis that increased exposure of the population to cadmium is associated with blood pressure elevation and with a higher prevalence of cardiovascular diseases.

Strenuous exercise has been claimed to modify renal glomerular and tubular function, the relative involvement of the two sites being unknown. These changes may be assessed by the determination of plasma high and low molecular mass proteins. A group of 13 man performed five runs (100, 400, 800, 1,500, 3,000 m) at maximal speed. The excretion rates and renal clearances of creatinine, albumin (Alb), beta 2-microglobulin (beta 2-m) and retinol-binding protein (RBP) were determined before and after each run. The glomerular filtration rate remained stable during the shorter runs and declined by about 40% during the longer runs. The excretion rate for Alb rose from 10-fold above the basal value (6 micrograms.min-1) for the 100 m to 49-fold for the 800 m and then declined for distances up to 3,000 m. The beta 2-m and RBP had a lesser initial increase, 3.5-(rest 55 ng.min-1) and 7.6-(rest 116 ng.min-1) fold, respectively, for the 100 m run and thereafter showed a higher excretion rate than Alb for the 400 m and 800 m runs. The renal clearances of these high (Alb) and low molecular mass (beta 2-m and RBP) proteins followed the changes observed for excretion rates. There was a linear relationship (r2 = 0.996) between plasma lactate concentration and total protein excretion in the postexercise period when taking all five runs into consideration. Glomerular permeability was primarily affected by the 100-m run while the longer runs modified both the glomerular and the tubular sites. To conclude, the present study demonstrated a differential response of the kidney to strenuous exercise with respect to the intensity and duration of the events.

The objective was to investigate the hypothesis that environmental exposure to cadmium may affect calcium metabolism in the population at large. The 1987 participants (965 men and 1022 women), from 20 to 80 years old, constituted a random sample of the population of four Belgian districts. The urinary excretion of cadmium, a measure of lifetime exposure, averaged 9-3 nmol/24 h in men (range 0 4-324 nmol/24 h) and 7-1 nmol/24 h (range 0-1-71 nmol/24 h) in women. Serum alkaline phosphatase activity and the urinary excretion of calcium correlated significantly and positively with urinary cadmium excretion in both men and women, and serum total calcium concentration negatively with urinary cadmium excretion in men only. The regression coefficients obtained after adjustment for significant covariates indicated that when urinary cadmium excretion increased twofold, serum alkaline phosphatase activity and urinary calcium excretion rose by 3-4% and 0 25 mmoll24 h respectively, whereas in men serum total calcium concentration fell by 6 umolIl.After adjustment for significant covariates the relation between serum total calcium concentration and urinary cadmium excretion was Cadmium interferes with the metabolism of vitamin D, calcium, and collagen, and its accumulation may lead to osteomalacia and osteoporosis.'2 These effects are usually considered to be late manifestations of severe cadmium poisoning, and have been seen in exposed workers and in malnourished subjects.'" The quantitative dose-response relation for the effects of cadmium on calcium and bone metabolism, however, remains presently unknown. The present report, part of a cross sectional study on the effects of cadmium on public health,"7 investigated whether environmental exposure to cadmium influences calcium metabolism in the population at large. Methods SUBJECTSAs described elsewhere,"7 the 2327 subjects (age range from 20 to 79) constituted a random sample of the population of four Belgian districts selected to provide a wide range of environmental exposure to cadmium. Subjects were excluded from the present analysis when not all relevant measurements were available (n = 248), when 24 hour urine samples were judged under or over collected by previously published criteria (n = 44),8 or when either occupational exposure to heavy metals (n = 41) or smoking habits (n = 7) could not be ascertained from a self administered questionnaire.

Cadmium is a cumulative environmental pollutant. For the general population mainly exposed by the oral route and through tobacco smoke inhalation, the kidney is the critical organ. Belgium is the principal producer of cadmium in Europe, and certain areas of the country are polluted by cadmium mainly because of past emissions from nonferrous industries. Preliminary studies carried out in one polluted area have suggested that environmental pollution might lead to an increased uptake of cadmium by the human body and possibly to health effects. Thus, a large-scale morbidity study has been initiated to assess the validity of this hypothesis. The present paper describes the protocol of this study. Its main objectives are to determine to what extent environmental exposure to cadmium resulting from industrial emissions may lead to accumulation of the metal in the human organism; to establish whether or not environmental exposure may induce renal changes and/or influence blood pressure; and to assess the acceptable internal dose of cadmium for the general population. The study design takes advantage of the fact that biological indicators of exposure, body burden, and early nephrotoxic effects of cadmium are available, which increase the likelihood of detecting a cause-effect relationship.