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Arch Environ Health. 1993 May-Jun;48(3):157-63.

Renal tubular function after reduction of environmental cadmium exposure: a ten-year follow-up.

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  • 1Department of Preventive Medicine and Health Promotion, Nagasaki University School of Medicine, Japan.


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.

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