Abstract:
Objective To investigate the effects of low-dose environmental cadmium exposure on human renal function and plasma transforming growth factor-β1 (TGF-β1) levels, and assess their relationship.
Methods A cross-sectional study design was used to select residents in a village with polluted irrigation history, where soil cadmium level was 2.30 mg/kg, as the exposed group, and residents in a village 32 km away without polluted irrigation history, where soil cadmium level was 0.22 mg/kg, as the control group. All the subjects had more than 5 years of local residency. Plasma TGF-β1, urinary cadmium, N-acetyl-beta-D-glucosaminidase (UNAG), albumin (UALB), and kidney injury molecule-1 (UKim-1) were detected. Non-parametric test and chi-square test were used to compare abnormal rate of renal injury. Pearson correlation analysis was used to assess the relationship of urinary cadmium with renal function and plasma TGF-β1, and multiple linear regression analysis was applied to analyze the influencing factors of renal function and plasma TGF-β1.
Results The urinary cadmium level of the exposed group was 1.06 μg/g (in terms of urinary creatinine, thereafter), higher than that of the control group (0.71 μg/g) (P < 0.001), and the levels were higher for both male and female in the exposed group (1.08 and 1.01 μg/g, respectively) than the same genders in the control group (0.73 and 0.70 μg/g, respectively) (P < 0.05). The levels of UNAG and UALB in the exposed group (17.40 U/g and 12.79 mg/g, respectively) were higher than those of the control group (14.80 U/g and 11.70 mg/g, respectively) (P < 0.05). With the increase of urinary cadmium levels, the abnormal rates of UNAG, UALB, and UKim-1 le vels increased significantly (χtrend2=19.945, 13.356, and 12.068, respectively, Ptrend < 0.05). The plasma TGF-β1 concentration of the exposed group (13.38 μg/L) was higher than that of the control group (10.11 μg/L) (P < 0.001). However, there was no difference in plasma TGF-β1 concentration among subjects grouped by different urinary cadmium levels (P > 0.05). The Pearson correlation analysis results showed that the urinary cadmium had positive correlations with UNAG, UALB, UKim-1, and age (r=0.14, 0.22, 0.10, and 0.19, respectively, P < 0.05). Plasma TGF-β1 was not associated with urinary cadmium, but positively with UNAG (r=0.12, P < 0.05). The multiple regression analysis results showed that urinary cadmium affected UNAG, UALB, and UKim-1 (b'=0.22, 0.25, and 0.15, respectively, P < 0.05).
Conclusion Environmental cadmium exposure could cause anomaly to renal function. With increased urinary cadmium levels, the abnormal rate of renal function is also obviously increased. Furthermore, there is a correlation between plasma TGF-β1 and UNAG. In the studied area, the cadmium exposure level is relatively low, and no relationship between urinary cadmium and plasma TGF-β1 is found.
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