Aim: To determine the effects of alcohol consumption and smoking on the onset of hypertension in a long-term longitudinal study. Methods: 7511 non-hypertensive male workers were enrolled. This cohort study was performed over an 8-year period using the results of the annual workers-health screening. The end-point was defined as systolic blood pressure ≥ 140 mmHg, diastolic blood pressure ≥ 90 mmHg, or use of antihypertensive drugs. For alcohol consumption, weekly alcohol intake (g ethanol/week) was estimated (1 “gou” = 22 g ethanol). Annual survey data were analyzed by pooled logistic regression that included alcohol consumption, smoking, age, body mass index, job schedule types, habitual exercise, and blood test measurements into the statistical model. Results: A significant positive dose–response relationship between alcohol consumption and onset of hypertension was observed, with synergistic health effects present. Compared with abstainers and nonsmokers, the adjusted odds ratios (95% confidence interval) for the onset of hypertension were: 1.51 (1.27–1.79) for 154 g ethanol/week and nonsmokers, and 1.81 (1.54–2.11) for 154 g ethanol/week and smokers. An interaction between alcohol and smoking was confirmed. Conclusions: This study provided information useful to the prevention of hypertension. By reducing alcohol consumption and smoking simultaneously, the risk of hypertension may be considerably lowered.

We investigated the biological half-life of urinary cadmium concentration (U-Cd) based on a 22-year follow-up study after cessation of environmental Cd pollution. Spot urine samples were obtained from the inhabitants (32 men and 36 women) in the target area in 1986, 1991, 1999, 2003 and 2008. These inhabitants were divided into higher or lower baseline U-Cd group by the cut-off of 5 μg l^–1 or 5 μg g^–1 creatinine. Biological half-life of U-Cd was estimated using a linear mixed model adjusted for the baseline age. In the higher baseline U-Cd groups, the estimated half-life and 95% confidence intervals were 12.4 years (9.3–18.8 years) and 11.4 years (9.3–14.6 years) for unadjusted U-Cd in men and women, respectively. For creatinine-adjusted U-Cd, they were 16.0 years (13.0–20.7 years) and 20.4 years (16.6–26.2 years) in men and women, respectively. In the lower baseline U-Cd groups, biological half-life for unadjusted U-Cd in men was solely significant (23.4 years) and longer than the corresponding half-life in the higher baseline U-Cd group. The biological half-lives of U-Cd obtained in this study were identical with the values for U-Cd or total body burden determined by a different method.

We aimed to investigate the mortality and causes of deaths of inhabitants with renal dysfunction induced by cadmium (Cd) exposure caused by heavy environmental contamination.

The aim of the present study was to estimate the benchmark doses (BMD) for renal effects for health risk assessment of residents living in Cd-polluted and non-polluted areas in a Thai population.