Iwata K, Saito H, Moriyama M, Nakano A
Department of Preventive Medicine and Health Promotion, Nagasaki University School of Medicine, Japan.
Arch Environ Health. 1993 May-Jun;48(3):157-63. doi: 10.1080/00039896.1993.9940814.
A prospective follow-up study was carried out to assess the prognosis of renal tubular function after reduction of environmental cadmium exposure. Time-related changes in urinary beta 2-microglobulin and cadmium excretion were followed from 1979 to 1989 in 102 residents of a cadmium-polluted area in Nagasaki, Japan. The average dietary cadmium intake among the study population was more than 200 micrograms/d in 1969, which decreased to approximately half that amount in 1983 because cadmium-polluted paddy fields were replaced with new soil in 1981. The geometric mean urinary beta 2-microglobulin concentration for 28 subjects aged 40 y or older in 1979 increased from 1,135.8 micrograms/g creatinine in 1979 to 1,999.7 micrograms/g creatinine in 1989. A similar tendency was also observed in 16 subjects with urinary beta 2-microglobulin concentrations greater than 1,000 micrograms/g creatinine in 1979, although the statistical significance of the difference did not reach the 5% level, probably because of the small sample size. In 48 persons examined in 1982, 1986, and 1989, the geometric mean of urinary cadmium concentration decreased from 8.49 micrograms/g creatinine in 1982 to 6.03 micrograms/g creatinine in 1989. The tendency for increasing beta 2-microglobulin excretion observed in the present study could not be explained by aging alone. Thus, it was concluded that renal tubular dysfunction caused by environmental cadmium was irreversible and slowly progressive, even after reduction of exposure. Six of 8 subjects who had severe renal dysfunction and who were included in the study died before 1986 and could not be followed. The implication of loss of subjects because of death is also discussed.
开展了一项前瞻性随访研究,以评估减少环境镉暴露后肾小管功能的预后。1979年至1989年期间,对日本长崎一个镉污染地区的102名居民的尿β2-微球蛋白和镉排泄的时间相关变化进行了跟踪。研究人群的平均膳食镉摄入量在1969年超过200微克/天,1983年降至该水平的约一半,因为1981年镉污染的稻田被新土壤取代。1979年,28名40岁及以上受试者的尿β2-微球蛋白几何平均浓度从1979年的1135.8微克/克肌酐增加到1989年的1999.7微克/克肌酐。1979年尿β2-微球蛋白浓度大于1000微克/克肌酐的16名受试者也观察到类似趋势,尽管差异的统计学显著性未达到5%水平,可能是因为样本量小。在1982年、1986年和1989年接受检查的48人中,尿镉浓度几何平均值从1982年的8.49微克/克肌酐降至1989年的6.03微克/克肌酐。本研究中观察到的β2-微球蛋白排泄增加趋势不能仅用衰老来解释。因此,得出的结论是,即使在减少暴露后,环境镉引起的肾小管功能障碍也是不可逆的且进展缓慢。研究中包括的8名患有严重肾功能障碍的受试者中有6人在1986年前死亡,无法进行随访。还讨论了因死亡导致受试者失访的影响。