低剂量环境镉暴露人群肾功能状况与血浆转化生长因子-β1的关系

Relationship between renal function and plasma transforming growth factor-β1 in population exposed to low-dose cadmium in environment

[目的]探讨低剂量环境镉暴露对肾功能和血浆转化生长因子-β1(TGF-β1)的影响,以及相互之间的关系。[方法]采用横断面研究,选择太原市有污染灌溉史且土壤镉含量为2.30 mg/kg的某自然村居民为暴露组,选择无污染灌溉史且与暴露组村落相距约32 km、土壤镉含量为0.22 mg/kg的某自然村居民为对照组。调查对象在当地的居住年限均大于5年。检测调查对象的血浆TGF-β1、尿镉、尿-N-乙酰-β-D-氨基葡萄糖苷酶(UNAG)、尿白蛋白(UALB)和尿肾损伤因子1(UKim-1)。分别用非参数检验、χ~2检验对肾损伤异常率进行比较,肾功能指标及血浆TGF-β1经对数转换后进行Pearson相关分析,影响因素采用多元线性回归分析。[结果]暴露组人群尿镉水平为1.06μg/g(以尿肌酐计,后同),高于对照组(0.71μg/g)(P<0.001),男性、女性尿镉水平(1.08、1.01μg/g)均高于同性别对照组人群(0.73、0.70μg/g,均P<0.05)。暴露组人群UNAG(17.40 U/g)、UALB(12.79 mg/g)均高于对照组(分别为14.80 U/g、11.70 mg/g)(均P<0.05)。随着尿镉水平的升高,UNAG、UALB、UKim-1的异常率升高(χ_(趋势)~2分别为19.945、13.356、12.068,均P_(趋势)<0.05)。暴露组血浆TGF-β1(13.38μg/L)高于对照组(10.11μg/L)(P<0.001),但不同尿镉水平人群血浆TGF-β1的差异无统计学意义(P>0.05)。Pearson相关分析结果显示:尿镉与UNAG、UALB、UKim-1和年龄均呈正相关关系(相关系数分别为0.14、0.22、0.10和0.19,均P<0.05);血浆TGF-β1与尿镉无相关性,与UNAG呈正相关关系(相关系数为0.12,P<0.05)。多元线性回归分析结果显示,尿镉对UNAG、UALB和UKim-1的变化影响较大(b'分别为0.22、0.25和0.15,均P<0.05)。[结论]环境镉暴露可引起肾脏功能的损害。随着尿镉水平增加,肾功能异常率也明显增加;且血浆TGF-β1与UNAG呈正相关。本研究所调查地区研究对象镉暴露水平相对较低,尚未发现尿镉与血浆TGF-β1之间的关系。

[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.