Bone resorption acceleration and calcium reabsorption impairment in a Thai population with high cadmium exposure.

Some residents of the Mae Sot district in Thailand have suffered long-term exposure to elevated dietary levels of cadmium. To test the hypothesis that chronic dietary cadmium exposure can cause imbalance in calcium dynamics and accelerate bone resorption, a group of these residents (156 men and 256 women aged >/= 50) were selected on the basis of previous records of elevated urinary cadmium and tested for urinary and blood cadmium, bone formation and resorption markers, and the renal tubular dysfunction markers. Both genders had high levels of blood and urinary cadmium and high urinary levels of the markers for renal dysfunction and bone resorption in a dose-response relationship to urinary cadmium. The excretion of bone resorption markers was positively correlated to the ratio of excreted calcium and urinary cadmium. The results of a multivariate regression analysis indicated that bone resorption was accelerated by impaired calcium reabsorption in renal tubules.

Monitoring of cadmium toxicity in a Thai population with high-level environmental exposure.

This study evaluated the utility of single and combined measurements of cadmium toxicity markers for surveillance purposes, using a sample of 224 individuals, 30-87 years of age, who were residents of cadmium polluted area in Mae Sot District, Tak Province, Thailand. Urinary cadmium levels excreted by them ranged between 1 and 58 microg/g creatinine with geometric mean of 8.2 microg/g creatinine which was 16-fold greater than the average for the general Thai population of 0.5 microg/g creatinine. The urinary markers evaluated were total protein, albumin, N-acetyl-beta-D-glucosaminidase (NAG), lysozyme, beta2-microglobulin (beta2-MG) and alpha1-microglobulin (alpha1-MG). Among these markers, only NAG showed a positive correlation with urinary cadmium in both male and female subjects with and without disease (r=0.43-0.71). Further, the prevalence rates for urinary NAG above 8 units/g creatinine (NAG-uria) increased with exposure levels in a dose dependent manner (p=0.05) among subjects with disease. In contrast, however, increased prevalence of beta2-MG above 0.4 mg/g creatinine (beta2-MG-uria) was associated with cadmium above 5 microg/g creatinine only in those without disease (POR=10.6 and 7.8 for 6-10 and >10 microg/g creatinine). Prevalence rates for abnormal excretion of all other markers, except albumin, were markedly increased among those having beta2-MG-uria with and without disease (chi2-test, p