Although contaminated rice appeared to be the main source of
Cd exposure among the residents in the present study, drinking
water might be another possible source. We provided in Table 4 the
urinary Cd levels of male and female subjects, stratified by drinking
water sources which included well, rain, and tap water. Only 18%
of subjects reported consuming bottle water and in both men and
women, urinary Cd levels in subjects who obtained drinking water
from wells were significantly higher than those who did not. Ageadjusted
mean urinary cadmium for male and female subjects who
consumed well water was 5.7 g/g vs. 6.1 g/g creatinine while the
corresponding value for male and female subjects who did not consume
well water was 3.7 g/g vs. 4.8 g/g creatinine, respectively.
The number of those subjects who sourced drinking water from
the river was only 5%, but urinary Cd levels of the consumers of
river water were higher than those of the non-river water-drinking
group, with a significant increase in women. Urinary Cd levels in
the groups with vs. without tap water and rainwater were similar
in both men and women.
3.2. Renal injury, renal tubular dysfunction and urinary Cd
Table 5 shows geometric means of 2-MG and NAG levels in
urine samples stratified by genders, age groups together with percent
of subjects with positive tests for urinary 2-MG ≥ 1000 g/g
creatinine or NAG ≥ 9 IU/g creatinine. The urinary 2-MG and NAG
levels among men and women in various age groups were staTable
5