Arisawa K, Nakano A, Saito H, Liu X J, Yokoo M, Soda M, Koba T, Takahashi T, Kinoshita K
Department of Preventive Medicine and Health Promotion, Nagasaki University School of Medicine, Sakamoto, Nagasaki, Japan.
Int Arch Occup Environ Health. 2001 May;74(4):255-62. doi: 10.1007/s004200000225.
This paper evaluates the associations of previous exposure to environmental cadmium (Cd) and renal function with total mortality and cancer incidence.
The study population comprised 275 residents (aged 40-92 years at baseline) in a Cd-polluted area located on Tsushima Island, Nagasaki, Japan. In the study area, the dietary intake of Cd decreased because the soil of the Cd-polluted rice fields was replaced with new soil between 1980 and 1983. The mortality rate from 1982 to 1997 and cancer incidence from 1985 to 1996 were investigated. Standardized mortality and incidence ratios (SMR and SIR) were calculated by using regional reference rates. The associations of renal function and urinary Cd levels with total mortality and cancer incidence were evaluated with Cox regression models.
The SMR for all subjects, and those with a urinary beta2-microglobulin (U-beta2M) concentration > or = 1,000 microg/g creatinine (Cr) and < 1,000 microg/g Cr was estimated at 90 [95% confidence interval (CI) 73-109], 138 (95% CI 101-183) and 66 (95% CI 49-87), respectively. After adjustment for age and other potential confounders, in men, serum beta2M (S-beta2M) (> or = 2.3 mg/l) and in women, serum Cr (> or = 21.2 mg/ 100 ml), relative clearance of beta2M (> or = 21%) and U-beta2M (> or = 1,000 microg/g Cr), were associated with a significantly increased risk of mortality, with hazard ratios exceeding 2.0. After further adjustment for log(U-beta2M), the rate ratio of deaths associated with, in men, increased S-beta2M was 2.53 (95% CI 0.97-6.65) and, in women, increased serum Cr (S-Cr) concentrations was 2.75 (95% CI 1.24-6.14). Urinary Cd concentrations (> or = 10 microg/g Cr) were not significantly associated with mortality. The overall SIR of all malignant neoplasms was 71 (95% CI 44-107).
These findings suggest that renal tubule dysfunction and a reduced glomerular filtration rate are predictors of mortality among persons previously exposed to environmental Cd. However, the results also suggest that overall mortality rates in Cd-polluted areas are not necessarily increased, because of the low mortality among those with no, or only slight, signs of low-molecular weight proteinuria. Overall cancer incidence may not be increased among residents in Cd-polluted areas.
本文评估既往环境镉(Cd)暴露及肾功能与总死亡率和癌症发病率之间的关联。
研究人群包括日本长崎对马岛一个镉污染地区的275名居民(基线年龄为40 - 92岁)。在研究区域,由于镉污染稻田的土壤在1980年至1983年间被新土取代,镉的饮食摄入量有所下降。调查了1982年至1997年的死亡率以及1985年至1996年的癌症发病率。使用地区参考率计算标准化死亡率和发病率比值(SMR和SIR)。采用Cox回归模型评估肾功能和尿镉水平与总死亡率和癌症发病率之间的关联。
所有受试者、尿β2 -微球蛋白(U -β2M)浓度≥1000μg/g肌酐(Cr)以及<1000μg/g Cr的受试者的SMR分别估计为90[95%置信区间(CI)73 - 109]、138(95%CI 101 - 183)和66(95%CI 49 - 87)。在调整年龄和其他潜在混杂因素后,男性血清β2M(S -β2M)(≥2.3mg/l)、女性血清Cr(≥21.2mg/100ml)、β2M相对清除率(≥21%)以及U -β2M(≥1000μg/g Cr)与死亡率显著增加相关,风险比超过2.0。在进一步调整log(U -β2M)后,男性中与S -β2M升高相关的死亡发生率比值为2.53(95%CI 0.97 - 6.65),女性中与血清Cr(S - Cr)浓度升高相关的为2.75(95%CI 1.24 - 6.14)。尿镉浓度(≥10μg/g Cr)与死亡率无显著关联。所有恶性肿瘤的总体SIR为71(95%CI 44 - 107)。
这些发现表明,肾小管功能障碍和肾小球滤过率降低是既往暴露于环境镉人群死亡率的预测因素。然而,结果还表明,镉污染地区的总体死亡率不一定会升高,因为无或仅有轻微低分子量蛋白尿迹象者的死亡率较低。镉污染地区居民的总体癌症发病率可能不会增加。