Very few studies have investigated the dose–response relationship between external cadmium (Cd) exposure and mortality. We aim to investigate the relationship between lifetime Cd intake (LCd) and mortality in the Cd-polluted Kakehashi River basin in Japan. Mortality risk ratios for a unit of increase of LCd and urinary Cd were analyzed using Cox’s proportional model. LCd was estimated based on residency and Cd in rice produced in their living areas. In men, mortality for all causes was significantly increased for a 10-μg/g Cr increase in urinary Cd, but not for a 1-g increase in LCd. In women, mortality risks for all causes and renal diseases, particularly renal failure, were significantly increased for a 10-μg/g Cr increase in urinary Cd. Similarly, mortality risks for renal diseases and renal failure were significantly increased for a 1-g increase of LCd in women. Comparing the contribution of two exposure markers to increased mortality in women, LCd was more effective for increasing mortality risks for renal diseases and renal failure, while urinary Cd contributed more to increased mortality risk for all causes. LCd may show a better dose–response relationship with mortality risk for renal diseases in women.

We evaluated the association between urinary cadmium concentration (uCd, μg/g Cr) and risk of cause-specific mortality according to urinary β2-microglobulin (MG) concentration. Participants were 1383 male and 1700 female inhabitants of the Cd-polluted Kakehashi River basin. The uCd and β2-MG were evaluated in a survey in 1981–1982, where those participants were followed-up over 35 years later. Among the participants with a urinary β2-MG < 1000, the hazard ratios (HRs) (95% confidence interval) for mortality were significantly higher in those with a uCd of ≥10.0 compared with <5.0 for cardiovascular disease [HR 1.92 (1.08–3.40) for men, 1.71 (1.07–2.71) for women], pneumonia or influenza [2.10 (1.10–4.00) for men, 2.22 (1.17–4.19) for women], and digestive diseases [for men; 3.81 (1.49–9.74)]. The uCd was significantly associated with mortality from heart failure in women and digestive diseases in men, after adjustment for other causes of death using the Fine and Gray competing risk regression model. For participants with a urinary β2-MG of ≥1000, no significant association was observed between uCd and any major cause of death. In the absence of kidney damage, Cd may increase the risk of death from cardiovascular disease, pneumonia, and digestive diseases.

The aim of the present study was to apply an updated benchmark dose (BMD) approach to estimate reference urinary cadmium (U-Cd) for renal tubular and glomerular effects. This cross-sectional survey was conducted 30 years ago in 30 men and 44 women living in a Cd-polluted area and in 18 men and 18 women living in a non-polluted area. We applied an updated hybrid approach to estimate the BMDs and 95% lower confidence limits (BMDLs) of U-Cd for creatinine (Cr) clearance (CrCl), estimated glomerular filtration rate (eGFR), β2-microglobulin (β2-MG), and β2-MG tubular reabsorption (%TRβ2-MG). Using a benchmark response (BMR) of 5%, we estimated the BMDLs of U-Cd for adverse renal effect markers to be 2.9 (eGFR), 1.8 (β2-MG), 1.8 (%TRβ2-MG < 95%), and 3.6 μg/g Cr (%TRβ2-MG < 90%) in men, and 3.5 (CrCl), 2.5 (β2-MG), 2.6 (%TRβ2-MG < 95%), and 3.9 μg/g Cr (%TRβ2-MG < 90%) in women. The obtained BMDLs for tubular effects were 1.8–3.6 µg/g Cr and for glomerular effects were 2.9–3.5 µg/g Cr; these are not very high compared to the exposure levels in the general population. The BMDLs calculated in this study provide important information for measures regarding protecting general inhabitants or workers from the adverse health effects of Cd exposure.

In this study, we measured the concentrations of polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) in the blood of 9-year-old children living in a dioxin hotspot area and a nonexposed area in Vietnam. Forty-five blood samples were collected in the hotspot area while twelve pooled blood samples were collected in the nonexposed area. We found that the dioxin level of children in the hotspot was significantly higher than that of children in the nonexposed area. The total TEQ of PCDD/Fs in the hotspot and the nonexposed was 10.7 and 3.3 pg TEQ/g fat, respectively. However, TCDD, the maker of Agent Orange, was not detected in the blood of children in the hotspot area. In the hotspot area, four congeners 1,2,3,4,6,7,8-HpCDD, 1,2,3,4,7,8-HxCDF, 1,2,3,6,7,8-HxCDF, and 1,2,3,4,6,7,8-HpCDF in mothers’ breast milk showed a significantly positive correlation with those in children’s serum although the correlations of 1,2,3,7,8-PeCDD and 2,3,4,7,8-PeCDF were not significant. In addition, the duration of breastfeeding also correlates with dioxins in children. These results suggested that children in the hotspot area were exposed to dioxin through mothers’ milk and other foods or environmental factors. The present study is the first study that shows dioxin levels in Vietnamese children.