Abstract
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.
Highlights
The kidney is a target organ of external cadmium (Cd), and renal tubular dysfunction is the most prevalent adverse health effect induced by Cd exposure
Nogawa et al (1989) [3] showed a prevalence of renal tubular dysfunction indicated by an increase in urinary β2–microglobulin (β2–MG) ≥1000 μg/g creatinine (g Cr) with increasing residential duration as well as RCd produced in the communities, suggesting that lifetime
In our previous studies, following-up subjects from the Kakehashi River basin who participated in health impact surveys in 1981–1982 for 9 and 15 years, we reported increased mortality for all causes, cardiovascular diseases, and renal diseases in the subjects with Cd-induced renal tubular dysfunction indicated by urinary β2-MG, protein, glucose, amino acids, and retinol-binding protein [7,8,9,10,11,12]
Summary
The kidney is a target organ of external cadmium (Cd), and renal tubular dysfunction is the most prevalent adverse health effect induced by Cd exposure. Significant associations between renal tubular dysfunction, indicated by increasing urinary low molecular protein and Cd exposure markers such as urinary Cd, were reported in residents of Cd-polluted areas in Japan [1]. Cd intake (LCd), defined from both factors of RCd and residential duration, is a useful indicator of external dose to show the dose–response relationship, with health effects induced by Cd exposure. In our previous studies, following-up subjects from the Kakehashi River basin who participated in health impact surveys in 1981–1982 for 9 and 15 years, we reported increased mortality for all causes, cardiovascular diseases, and renal diseases in the subjects with Cd-induced renal tubular dysfunction indicated by urinary β2-MG, protein, glucose, amino acids, and retinol-binding protein [7,8,9,10,11,12]. An investigation of the relationship between the urinary Cd levels and mortality in the 15- and 22-year follow-up studies showed increased mortality for all causes, including renal diseases and heart failure, among subjects with urinary Cd levels ≥10 μg/g Cr in the 1981–1982 survey compared with subjects with Cd levels
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