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Cadmium is a well-known nephrotoxic agent with extremely long biological half-time of 10-30 years in human. To investigate the evolution of cadmium-induced renal effects in the population, a number of 148 residents who lived in cadmium-polluted area were followed-up for 3 years after the reduction of cadmium exposure in rice. Urinary cadmium (UCd), beta(2)-microglobulin (B2M) and albumin (ALB) were analyzed in 1995 and 1998, respectively. The results demonstrated that the changes of renal effects of residents depended on the levels of UCd before inflow of cadmium to human body declined. In cases where UCd were less than 10 microg/g creatinine in 1995, evidence was found indicating significant decreases in proteinuria (i.e., B2M and ALB) 3 years later, whereas, in cases where the excretion of UCd exceeded 10 microg/g creatinine in 1995, progression was observed. The study of dose-response relationships between UCd and B2M or ALB also showed that the cadmium-induced renal dysfunction might be reversible if UCd concentration was low-level before exposure decreasing, otherwise it might be irreversible or aggravated.

The objective of this study was to investigate the possible effects of environmental cadmium (Cd) exposure on the levels of serum sex hormones in a Chinese population group. A total of 263 male volunteers were included. Blood samples were collected for the determination of serum testosterone (T), measured by radioimmunoassay, and follicle stimulating hormone (FSH) and luteinizing hormone (LH), both measured by enzyme immunoassays. Urinary and blood Cd were analyzed by atomic absorption spectroscopy (AAS). We found a dose-response relationship between urinary Cd excretion and the prevalence of abnormally high serum T levels, but, through multiple regression analysis, we could not trace exposure to Cd as a significant determinant of serum T levels. Exposure to Cd also failed to influence the levels of FSH and LH in serum. In contrast, we found that age, body mass index (BMI), and smoking habits are significant determinants of FSH and LH and of T and LH, respectively. We conclude that oral Cd exposure is not a critical determinant of hormone homeostasis in males, but lifestyle and some biological factors, such as age and BMI, are important. The relationship found between urinary Cd and high T levels may be of importance for male reproductive morbidity and should be investigated further.

Osteoporosis is a common metabolic disease characterized by low bone mass and microarchitectural deterioration of bone tissue. Many factors are involved in the occurrence of osteoporosis. Cadmium can cause both osteomalacia and osteoporosis and these effects have long been investigated through various epidemiological or experimental studies. The present study examines a possible relationship between cadmium nephropathy and its effects on the skeleton in populations living in a polluted area in southeast China. Monophoton absorptiometry was used to measure bone mineral density in the population and the Z score (the number of SD from the difference between the measured bone density of the individual and the group mean value for sex- and age-matched controls) was introduced to define osteoporosis (Z score < -2). Osteoporosis caused by cadmium exposure was demonstrated in this study on a general population environmentally exposed to cadmium in China. It was found that there were significant differences in the prevalence of osteoporosis among the different urinary cadmium groups (chi2 = 18.84, P = 0.0008). The linear trend test gave chi2 = 16.281, P = 0.00005. There was a dose-response relationship between cadmium exposure (urinary cadmium) and prevalence of osteoporosis. Of 31 subjects with osteoporosis, 23 subjects were suffering from renal dysfunction. The prevalence of renal dysfunction (74.19%) was significantly higher than that in those without osteoporosis (chi2 = 16.53, P < 0.001). Stratum analysis was performed to further assess the relationship between bone damage and renal impairment caused by cadmium. There was a significant difference between those with and without tubular damage (chi2 = 19.92, P = 0.000) but not in those with and without glomerular damage (chi2 = 0.08, P = 0.114). This showed that glomerular dysfunction plays a smaller role than tubular dysfunction in the causation of bone damage. It was found that the prevalence of osteoporosis increases with increasing values of parameters of tubular damage. Osteoporosis caused by cadmium is thus related to kidney dysfunction and especially to tubular damage and its severity but not to glomerular damage. The present study has thus demonstrated the combined adverse effects (osteoporosis and renal dysfunction) caused by environmental exposure to cadmium for the first time in Asia outside the endemic area in Japan.

Human exposure to cadmium may occur in both occupational and general environments. We were interested in determining whether a combination of occupational and environmental exposure to cadmium results in different levels of severity of renal dysfunction relative to that arising from environmental or occupational exposure alone. We selected 44 residents, who once were employed in a smelter and lived in a cadmium-polluted area, as group A. Another 88 subjects, who never worked in the plant, but lived in the same area, were selected as group B. Group C consisted of 88 subjects who had no history of occupational exposure to cadmium and lived in a non-cadmium-polluted area. Statistical analysis demonstrated that there was no significant difference in age or gender among the three groups, nor were there significant differences in smoking habits. The prevalence of renal dysfunction as indicated by increased excretion of beta2-microglobulin (B2M), N-acetyl-beta-D-glucosaminidase (NAG) and albumin (ALB), was higher in group A than in group B. This finding suggests that exposure to cadmium both occupationally and environmentally results in a higher prevalence of renal dysfunction, relative to those who are exposed to cadmium only in the general environment. Therefore, this specific population, who once were occupationally exposed to cadmium and lived in polluted areas, should be identified. Furthermore, health examinations of this population should be conducted in time to prevent further health damage induced by cadmium exposure.

To explore possible effects of environmental cadmium exposure on prostate in humans, and the possible relationship of serum sex hormones to occurrence of clinic signs of tissue changes in the prostate, a case-control study was undertaken in the southeast part of China in 1998. A total of 297 male volunteers from a control area and two cadmium-polluted areas were included as subjects in this study. All the subjects were required to answer a questionnaire and to undergo a complete physical examination including digital-rectal examination (DRE). Blood and urine samples were collected. Serum total prostate specific antigen (PSA), total serum testosterone (T), follicle stimulating hormone (FSH) and luteinizing hormone (LH) were measured by radioimmunoassay and enzymeimmunoassay method, respectively. The data of urinary cadmium (U-Cd) and blood cadmium (B-Cd) were obtained by atomic absorption spectrometry (AAS) as an indicator of cadmium body burden. Statistical analysis was applied to investigate a possible relation between cadmium exposure and prostate pathological changes. The results show that there is a clear dose-response relationship between cadmium exposure and the prevalence of cases with abnormal PSA. The blood cadmium content in cases with positive DRE was significantly higher than that of subjects with negative DRE (P < 0.05). Significant differences in the level of FSH between cases with positive DRE and the normal subjects were also noted (P < 0.05). These results indicate that chronic environmental cadmium exposure is associated with injuries to human prostate. A possible relationship to changes in circulating sex hormones needs further investigation.

We have performed a study aimed at investigating the critical concentration of urinary cadmium (UCd) required for the development of renal dysfunction. We studied population groups (totally 790 persons) living in two cadmium exposed areas and one control area in China. UCd, was determined as an indicator of cadmium exposure and accumulation, while the concentrations of N-acetyl-beta-D-glucosaminidase (NAG), its iso-form B (NAG-B), beta2-microglobulin (B2M), retinol binding protein (RBP), and albumin (ALB) in urine were measured as indicators of the renal effects caused by cadmium. There was a significantly increased prevalence of hyperNAGuria, hyperNAG-Buria, hyperB2Muria, hyperRBPuria and hyperALBuria with increasing levels of Cd excretion in urine. We used the benchmark dose (BMD) procedure to estimate the critical concentration of urinary cadmium in this general population. The lower confidence limit of the BMD (LBMD-05) of urinary cadmium for a 5% level of risk above the background level was estimated for each of the renal effect indicators. The BMD-05/LBMD-05 were estimated to be 4.46/3.99, 6.70/5.87, 8.36/7.31, 7.98/6.98 and 15.06/12.18 microg/g creatinine for urinary NAG-B, NAG, B2M, RBP and ALB, respectively. Our findings suggest, based on the present study, that the Lower Confidence Limit of the Population Critical Concentration of UCd (LPCCUCd-05) of tubular dysfunction for 5% excess risk level above the background may be ca. 3-4 microg/g creatinine, and that cadmium concentration in urine should be kept below this level to prevent renal tubular damage. This report is the first to use the BMD method in this field and to define the concept of critical concentration in urine.

This paper presents the main findings of a study on health effects of environmental cadmium pollution in China, performed in 1998, i.e. approximately 25 years after the first warnings of such effects were published in Ambio. Forearm bone mineral density (BMD) and renal dysfunction were assessed in population groups exposed to cadmium via rice. Decreased BMD was found in postmenopausal women with elevated urinary cadmium (CdU) or cadmium in blood (CdB) and among men with elevated CdB. Also, clear and statistically significant dose-effect and dose-response relationships were found between CdB or CdU and renal dysfunction (increased excretion of retinol-binding protein). This is the first report of bone effects among Cd-exposed population groups in Asia outside Japan. The report is also of interest since it demonstrates that bone effects, a comparatively severe adverse health effect of Cd, in combination with renal dysfunction, still occurs in environmentally exposed population groups in Asia. Recent reports on bone effects in Cd-exposed population groups in Europe are discussed.