Cadmium and Other Metal Levels in Autopsy Samplesfrom a Cadmium Polluted Area and Non polluted Control Areas in Japan

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Cadmium and Other Metal Levels in Autopsy Samples
from a Cadmium-Polluted Area and Non-polluted Control
Areas in Japan

Chiyo Hayashi

&

Naoko Koizumi

&

Hisahide Nishio

&

Naoru Koizumi

&

Masayuki Ikeda

of cadmium (Cd) and other metals in kidney and liver in
autopsy samples and to compare the levels between those in
an area with heavy Cd exposure and those in no-polluted
areas in Japan. Data on Cd and other metals in kidney
(cortex and medulla) and liver in 95 cases (87 women and
eight men; the exposed) in a Cd-polluted area and 43 cases
(21 women and 22 men; the controls) in non-polluted areas
were cited from 15 previous publications to be summarized
together with six unpublished cases. Cd levels in kidney
cortex and medulla were significantly lower in the exposed
(31.5 and 23.8

μg/g wet tissue as GM, respectively) than in

the controls (82.7 and 36.4

μg/g, respectively), whereas Cd

levels in liver was higher in the exposed (60.2

μg/g) than in

the cortex (29.9

μg/g) and medulla (22.7 μg/g) than

exposed men (55.4 and 38.1

μg/g, respectively) as well as

in cortex of control women (92.9

μg/g). Comparison with

worldwide data other than Japan for non-exposed popula-
tions [19.1, 9.3, and 1.3

μg/g in cortex, medulla, and liver,

respectively, as the inverse variance-weighted averages
(IVWA) of GM values for each of 22 reports] suggests that
the levels for the non-exposed Japanese (123.3, 33.5, and
3.9

μg/g as IVWA) tended to be higher than the levels in

other countries, possibly reflecting high dietary Cd intake in
the past.

Keywords Autopsied samples . Cadmium . Cupper.
Kidney. Lead . Liver. Zinc

Introduction

Cadmium (Cd) is a ubiquitous environmental pollutant,
known to be toxic predominantly affecting proximal tubules
in kidney and bone after long-term exposures [

1

]. Separate

from occupational Cd exposure, non-occupational expo-
sures occur typically via intake of Cd-polluted foods and
drinking water [

2

4

]. In cases of Itai-itai disease (a typical

chronic Cd poisoning) along the Jinzu River basin in Japan,
the toxic effects involved severe damage of renal tubulop-
athy coupled with osteomalacia [

5

]. Although no exact

report on exposure intensity of the patients was available, a
survey in the basin in 1968 showed that the dietary
exposure among the local population at the time of survey
was about 600

μg/day or even higher [

4

]. Cd has a long

C. Hayashi

:

H. Nishio

Department of Public Health, Kobe University Graduate School
of Medicine,
Kobe 650-0017, Japan

N. Koizumi
Food Safety Commission, Cabinet Office, Government of Japan,
Tokyo 107-6122, Japan

N. Koizumi
School of Public Policy, George Mason University,
Arlington, VA 22201, USA

M. Ikeda (

*)

Kyoto Industrial Health Association,
67 Nishinokyo-Kitatsuboicho, Nakagyo-ku,
Kyoto 604-8472

( Kyoto, Japan

e-mail: ikeda@hokenkai.jp

Biol Trace Elem Res (2012) 145:10

–22

DOI 10.1007/s12011-011-9155-1

Received: 3 February 2011 / Accepted: 15 July 2011 / Published online: 2 August 2011

# Springer Science+Business Media, LLC 2011

Abstract This study was initiated to examine accumulation

the controls (8.1

μg/g). Exposed women had lower Cd in

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biological half-life of 10 or more years [

1

] to stay long in

the body once absorbed.

Analysis of autopsy tissue samples has been conducted

worldwide since 1970s [

6

,

7

], in order to investigate the

extent of accumulation in human body. In Japan in
particular, continuous efforts have been made especially
on those in a Cd-polluted area including Itai-itai disease
victims, and the results of analyses have been reported by
various authors (for details, see the

Materials and

Methods

section). The latest review reports have been

published in 1986 [

8

] and 1990 [

9

] with no follow-up since

then.

It is the purpose of the present study to compile

recent observations. Thus, by citation from 15 previous
publications combined with six unpublished cases, 95
cases from a Cd-polluted area were summarized in the
present report together with 43 cases from areas with no
apparent pollution with Cd, and the extent of accumu-
lation of Cd in kidney cortex, kidney medulla, and liver
was compared between the exposed and non-exposed
cases. Levels of zinc (Zn), lead (Pb), and copper (Cu)
were also reported as the metals of toxicological interest
[

2

,

3

,

9

11

].

Materials and Methods

Materials

Data on Cd, Cu, Pb, and Zn in kidney (cortex and
medulla) and liver (right lobe) of autopsied samples of
Itai-itai disease patients and the patients suspected of
the disease in Jinzu River basin [the exposed

—95 cases

(87 women and eight men)] and controls [the controls

43 cases (21 women and 22 men)] in non-polluted areas
were cited from 15 previous publications that cover all
of related articles on autopsy cases in Japan till 2007
[

12

26

]. Findings in six unpublished cases were also

combined together (Table

1

). It should be noted that the

Itai-itai disease victims were predominantly women (i.e.,
192 women and three men among 195 government-
recognized Itai-itai disease patients and 289 women and
47 men among 336 suspected cases [

27

]), and as a result,

the autopsy cases were mostly women. The causes of
death of the control group were ischemic heart disease,
cancers (lung, gall bladder, stomach, pancreas, or liver),
brain tumor, and brain thrombosis [

12

]; the causes of

death were similar also for control cases recorded in later

Table 1 List of databases

References cited

Exposed

Controls

Age range (years) No. of cases

Cd (GM;

μg/g wet tissue)

a

Age (years) No. of cases

Cd (GM;

μg/g wet

tissue)

a

Kidney

Liver

Kidney

Liver

Total Gender

Cortex

Medulla

Total Gender

Cortex Medulla

Kuzuhara et al. [

12

] 62

–94

44

W37, M7 34.8

26.2

73.3

57

–87

17

W11, M6

87.7

35.5

7.8

Kuzuhara et al. [

13

] 69

–87

5

W

35.6

27.3

46.5

35

–78

8

W3, M5

95.3

43.6

10.2

Kuzuhara et al. [

14

] 70

–83

7

W

41.6

27.8

61.8

Kuzuhara et al. [

15

] 74

–85

7

W

31.2

23.1

63.4

Kuzuhara et al. [

16

]

46

–73

3

W2, M2

66.8

31.6

3.6

Kuzuhara et al. [

17

] 77

–97

6

W

28.3

23.4

34.2

46

–81

14

W5, M9

91.0

36.8

9.3

Kuzuhara et al. [

18

] 71

–889

3

W

22.3

17.2

43.7

72

1

W

5.7

3.8

22.2

Kuzuhara et al. [

19

] 82, 87

2

W

22.3, 30.4 11.7, 19.7 34.4,25.2

Kuzuhara et al. [

20

] 75, 88

2

W

35.9, 40.5 29.3, 25.5 16.5, 30.2

Kuzuhara et al. [

21

] 84, 79

2

W

9.5, 46.1

11.1, 36.6 117, 69.4

Nogawa et al. [

22

]

90

–91

3

W

20.7

14.8

71.1

Nogawa et al. [

23

]

87, 87

2

W

11.9, 35.6 8.1, 19.8

40.0, 90.5

Nogawa et al. [

24

]

90

1

W

27.0

28.6

120

Nogawa et al. [

25

]

83, 88

2

M

30.1, 27.9 25.0, 14.7 76.9, 47.1

Nishio et al. [

26

]

95

3

W

22.6

21.1

50.0

Unpublished data

66

–88

6

W

34.5

22.4

43.3

Total

62

–95

95

W87, M8 31.5

23.8

60.2

35

–87

43

W21, M22 82.7

36.4

8.1

W women, M men

a

Individual values are given when a number of cases are two or less

Cadmium and Other Metal Levels in Autopsy Samples

11

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years. Of the database, attention was focused to metal
levels in kidney and liver, the two organs of toxicological
importance.

Instrumental Analyses for Metals

As described by Kuzuhara et al. [

12

], each tissue [fresh and

unfixed (e.g., in formalin), 1

–10 g wet weight] was

mineralized by heating in the presence of 12 N nitric acid
to dryness, and the residue was taken up in 1 N nitric acid.
The final preparation was subjected to instrumental analy-
ses for Cd, Cu, and Pb with a graphite furnace atomic
absorption spectrometer (GFAAS) at 228.8, 324.7, and
283.3 nm, respectively, and for Zn with a flame atomic
absorption spectrometer at 213.8 nm (Hitachi Z-8200, 180-
70 or 180-80, Hitachinaka, Japan). Later cases were treated
also after this protocol.

A bovine liver standard reference material (NIST SRM

1577c) was analyzed for reference. When the material was
analyzed ten times, the accuracy (i.e., the ratio in
percentage of the mean measured values/the certified
values) and the precision (as the coefficients of variation
in percent; given in parentheses) were 95.4% (1.75%) for

Cd, 97.2% (3.29%) for Cu, 94.3% (2.15%) for Pb, and
97.7% (1.49%) for Zn. Thus, the accuracy/precision of the
methods employed was considered satisfactory, and no
adjustment of the measured values was made. For the sake
of better quality control, results of measurements made in a
single laboratory (Department of Public Health, Kobe
University Graduate School of Medicine, Kobe, Japan)
were selectively cited so that all measurements were
conducted by a single analytical chemist (C.H.) in the
laboratory.

Statistical Analysis

A normal distribution was assumed for age. Log-normal
distributions were assumed for metal concentrations in
tissues, by analogy to the cases of the metals in blood [

28

,

29

], in urine [

30

,

31

], and in daily food [

2

,

4

]. Accordingly,

age was expressed in terms of arithmetic mean and
arithmetic standard deviation (AM±ASD) and metals were
in geometric mean and geometric standard deviation [GM
(GSD)]. In some of publications collected, metal levels
were originally expressed in terms of AM±ASD, and GM
and GSD were estimated by use of the moment method

Element

Group

Parameter

Metal (

μg/g)

Kidney

Liver

Cortex

Medulla

Cd

Exposed

GM

31.5

23.8

60.2

GSD

1.79

1.64

1.94

Controls

GM

82.7

36.4

8.1

GSD

1.99

1.99

2.66

p for difference

↓↓

↓↓

↑↑

Cu

Exposed

GM

1.6

1.4

3.8

GSD

1.49

1.51

1.84

Controls

GM

2.6

2.0

6.1

GSD

1.80

1.52

1.87

p for difference

↓↓

↓↓

↓↓

Pb

Exposed

GM

0.08

0.09

0.27

GSD

1.91

1.87

2.79

Controls

GM

0.09

0.08

0.14

GSD

1.67

1.68

1.69

p for difference

ns

ns

↑↑

Zn

Exposed

GM

30.1

23.2

112.7

GSD

1.37

1.32

1.45

Controls

GM

56.4

34.3

74.5

GSD

1.54

1.51

1.83

p for difference

↓↓

↓↓

↑↑

Table 2 Levels of Cd, Cu, Pb,
and Zn in various organs; com-
parison between the exposed
and the controls

In total, 95 exposed (87 women
and eight men) and 41 controls
(21 women and 21 men) were
studied. Unpaired t test was
applied after log-conversion of
values. Upward and down
arrows show significant increase
or decrease, respectively, in the
exposed as compared with the
levels in the controls (two
arrows for p<0.01). ns for
p>0.10

12

Hayashi et al.

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after Sugita and Tsuchiya [

32

] for uniformity in data

presentation. Thus, inverse variance-weighted average
(IVWA) was calculated as:

Log IVWA

ð

Þ ¼ Σ Log GM

i

½

Þ= Log GSD

i

ð

Þ

2

=Σ½1= Log GSD

i

ð

Þ

2

i ¼ 1 to n

ð

Þ:

Differences in means between the cases and controls

(women and men separately or in combination) were
examined by unpaired t test (after logarithmic conversion)
when a whole of the exposed cases was compared with a
whole of the control cases and by paired t test when 16
exposed cases were matched by age with an equal number
of controls. Simple regression analyses were also applied.
When two regression lines were compared, statistical

significance of the difference in the intercepts, the slopes,
and the correlation coefficients was examined after Ichihara
[

33

].

Results

Age Distribution of Exposed and Control Groups by Sex
and Combination

When age distributions were compared between the
exposed and controls, the exposed (women and men,
separately and as combined) were significantly (p<0.05)
older than corresponding controls. No significant (p

≧0.05)

difference in age was detected between women and men in
the exposed and also in the controls.

Groups (number of cases)

Parameters

Cd (

μg/g)

Kidney

Liver

Cortex

Medulla

Exposed, total (n=95)

GM

31.5

23.8

60.2

GSD

1.79

1.64

1.94

Max

123

82.4

287

MED

29.3

22.6

58.5

p for difference from total controls

↓↓

↓↓

↑↑

Exposed women (n=87)

GM

29.9

22.7

57.7

GSD

1.75

1.62

1.93

Max

123

82.4

287

MED

28.2

22.4

55.1

p for difference from control women

↓↓

↓↓

↑↑

p for difference from exposed men

↓↓

↓↓

Exposed men (n=8)

GM

55.4

38.1

94.2

GSD

1.61

1.38

1.77

Max

105

65.9

201

MED

57.8

39.9

98.3

p for difference from control men

ns

ns

↑↑

Controls, total (n=43)

GM

82.7

36.4

8.1

GSD

1.99

1.99

2.66

Max

218

111

49.6

MED

86.3

39

8.7

Control women (n=21)

GM

92.9

38.4

11.4

GSD

2.11

2.15

1.99

Max

218

111

49.6

MED

104

43.4

10.7

p for difference from control men

ns

ns

Control men (n=22)

GM

74.1

34.6

5.8

GSD

1.87

1.86

3.02

Max

193

91.6

35.1

MED

75.6

38.7

7.3

Table 3 Comparison of Cd in
kidney and liver between the
exposed and the controls of two
sexes

Arrows (including directions)
are as under Table

2

. One arrow

for p>0.05, and ns for p>0.1.

Cadmium and Other Metal Levels in Autopsy Samples

13

background image

Metal Levels in Kidney and Liver in Exposed Cases
in Comparison with the Levels in Controls

GM and GSD values for Cd, Cu, Pb, and Zn in kidney
(separately for cortex and medulla) and liver of the exposed
and controls were summarized in Table

2

, together with

results of comparison between the exposed and the controls.
Cd, Cu, and Zn were substantially (p<0.01) lower in kidney
(both in cortex and in medulla) of the exposed as compared
with the levels in the controls; in case of Cd, the levels in the
cortex of the exposed were less than a half of the controls,
and it was about 65% in the medulla. In contrast, Cd, Zn,
and also Pb in liver of the exposed were much higher (p<
0.01) than the levels for the controls. The behavior of Zn in
the tissues was similar to that of Cd. Trends of changes in Pb
was different from that of Cd in the sense that Pb in kidney
cortex and medulla of the exposed was similar to that of the
controls, although the levels in liver of the exposed was
almost twice as high as the levels of the controls (p<0.01).

Comparison of Cd in Kidney and Liver
Between the Exposed and the Controls
and Between the Two Sexes

Breakdown into two sexes (Table

3

) showed that exposed

women had lower Cd in both cortex (p < 0.01) and medulla

(p < 0.01) and higher Cd in liver (p < 0.01) than control
women. The reverse was the case for Cd in liver. When
compared with Cd in exposed men, exposed women had
lower Cd (e.g., p < 0.01 in cortex) than exposed men,
although the number of cases of exposed men was as
small as eight. Interestingly, there was no significant
difference (p > 0.05) in Cd in cortex and medulla between
the two groups of the exposed and control men, although
the levels in liver were higher (p < 0.01) in exposed men
than in control men.

Comparison on Cd and Other Metal Levels Between 16
Paired Cases of Women

Further attempts were made to confirm differences in metal
levels between the exposed cases and controls. Because age
distributions were not similar between the exposed and the
controls, age-matched pairs were selected (with an allow-
ance of 2 years) between the two groups. In practice, 16
pairs (13 pairs for women and three pairs for men) were
available (Table

4

), with no significant difference in age

distribution (p>0.1).

Statistical evaluation showed that Cd was lower in cortex

and higher in liver of the exposed cases as compared with the
levels in controls, whereas no significant difference (p>0.1)
was detected in Cd in medulla. The behavior of Zn was close

Table 4 Comparison of element levels in kidney and liver between 16 age-matched pairs

Groups

Age

Cd (

μg/g)

Cu (

μg/g)

Pb (

μg/g)

Zn (

μg/g)

Kidney

Liver

Kidney

Liver

Kidney

Liver

Kidney

Liver

Parameters

Cortex

Medulla

Cortex

Medulla

Cortex

Medulla

Cortex

Medulla

Exposed

GM

76.1

a

39.3

30.5

62.0

1.8

1.7

4.1

0.10

0.09

0.42

32

26

122

GSD

7.2

a

2.01

1.84

1.93

1.76

1.64

1.90

1.44

1.51

2.93

1.49

1.36

1.42

Min

62

16.9

12.2

16.1

0.7

0.8

1.5

0.06

0.04

0.09

18

17

47

Max

87

123.0

82.4

128.0

9.0

6.5

11.8

0.20

0.21

3.59

82

53

193

MED

75

36.9

29.6

76.9

1.7

1.6

4.1

0.09

0.09

0.41

32

24

129

Controls

GM

75.9

a

93.5

39.6

11.3

2.1

1.7

5.4

0.10

0.08

0.16

53

31

88

GSD

7.0

a

1.71

2.04

2.33

1.48

1.32

1.78

1.78

1.68

1.62

1.63

1.63

1.76

Min

64

27.1

9.6

2.6

0.9

1.1

2.2

0.04

0.04

0.07

22

18

27

Max

87

215.0

111.0

49.6

3.5

3.1

19.8

0.33

0.31

0.38

158

92

200

MED

75

85.6

47.2

14.0

2.3

1.5

5.7

0.10

0.08

0.15

55

27

95

p for difference

ns

b

↓↓

ns

b

↑↑

ns

b

ns

b

ns

b

ns

b

ns

b

↓↓

ns

b

ns

c

Arrows (including directions) and ns are as under Tables

2

and

3

; 16 pairs (13 pairs for women and three pairs for men) were compared

a

AM and ASD in case of age

b

ns for p>0.1

c

ns for 0.05<p<0.1

14

Hayashi et al.

background image

to that of Cd in the sense that the levels were lower in kidney
cortex (p<0.01) with no difference in medulla (p>0.1). Cu
and Pb showed no similar behavior with Cd (Table

4

).

Possible Difference in the Effects of Aging in Cd
Between the Exposed and the Controls

Possible effects of aging on Cd in cortex, medulla, and liver
were examined by regression analysis, taking age as an
independent variable and Cd levels in the tissue a
dependent variable. Only women were selected as sex
difference was detected in Cd in the tissues (Table

3

), so

that 87 exposed women and 21 control women were
subjected to the analysis. Analyses were made with Cd
levels as measured (i.e., without logarithmic conversion)
and also after logarithmic conversion.

The slopes were negative (i.e., <0) in cases of Cd in

cortex and medulla and positive (i.e., >0) for Cd in liver.
The correlation coefficients were, however, small (|0.3| at
best), and none of them was statistically significant,
irrespective of application of logarithmic conversion. No
significant difference was detected in regression lines
possibly because the correlation was poor with small
correlation coefficients. The regressions are presented in
Fig.

1

for visual understanding of the cases.

Discussion

The present analysis gave two major findings that Cd in
kidney cortex was lower in the exposed than in the controls
and that Cd in liver of the exposed was higher than that in
the liver of the controls as well as in the cortex of the
exposed. Age-dependent increase in Cd in cortex could not
be confirmed both in the exposed and the controls (Tables

3

and

4

; Fig.

1

). Takebayashi et al. [

34

] also observed that Cd

in liver was higher than that in kidney cortex among the
autopsy samples from 11 subjects (the two sexes combined)
in Tsushima Island, another Cd-polluted area in Japan,
separate from the current study region of Jinzu River basin.
Unfortunately, no control cases were reported. Neverthe-
less, it should be worthy to note that both Cd in liver
(75.5

μg/g as GM) and in kidney cortex (36.5 μg/g)

reported by Takebayashi et al. [

34

] were even higher than

the present findings (60.2 and 31.5

μg/g in liver and in

kidney cortex, respectively; Table

2

).

In reviewing previous publications, some of authors in

1970s reported the Cd levels in dry tissue [

35

37

] or dry

ash of the tissue [

38

,

39

]. Some others reported Cd in

formalin-fixed tissue samples. Such data were considered to
be inappropriate for comparison with the levels in fresh wet
tissue. Furthermore, only cases with flame AAS, GFAAS,
and inductively coupled mass spectrometry (ICP-MS) as

methods of analyses were in Table

5

and the

Appendix

(e.g., the results with other methods such as neutron
activation [

40

] or X-ray fluorescence [

41

] were not in the

table to reduce possible difference between the methods
employed). Thus, Cd levels in kidney and liver on a fresh
wet weight basis were available in 27 publications [

8

,

9

,

42

66

] on kidney cortex, kidney medulla, and liver in 48,

5, and 56 groups of subjects who had no occupational or
environmental pollution-induced Cd exposures (Table

5

;

for details, see

Appendix

). In addition, Cd in kidney

(without identification of cortex or medulla) was available
in 38 groups. The number of cases in a group was various
from two (for 45

–54-year-old subjects [

43

] or 30

–39-year-

old women [

55

]) to 2,659 cases [

56

]. The inverse

variance-weighted averages of the reported (or estimated)
GM values are shown in the bottom of Table

5

together

with the minimum and the maximum values. Comparison
with the present findings (GMs) in non-exposed controls (also
cited in the bottom of the table) reveal that the values for cases
in Japan without environmental pollution (i.e., non-exposed

Age (years)

Cd in kidney cortex (µg/g wet tissue)

0

25

50

75

100

125

150

175

200

225

45

50

55

60

65

70

75

80

85

90

95 100

0

25

50

75

100

125

150

175

200

225

45

50

55

60

65

70

75

80

85

90

95 100

A

B

Fig. 1 Poor correlation of Cd in kidney cortex with age. a
Exposed women (n = 87), b Control women (n = 21). The line in the
middle is a calculated regression line, and two dotted curves on both
sides show the 95% confidence interval for the means. Each dot
represents one case. The equation for the regression line in the top
figure of a is Y= 59.1

–0.295× (r=−0.088, p>0.1) and that in the

bottom figure of b is Y= 134.2

–0.360× (r=−0.088, p>0.1)

Cadmium and Other Metal Levels in Autopsy Samples

15

background image

controls) were apparently higher than the levels for popula-
tions in areas other than Japan, irrespective of cortex, medulla,
or liver. Such was also the case even when only adult
populations (selected from [

43

,

45

,

46

,

48

52

,

55

,

57

59

,

61

,

62

,

64

66

]) were compared between those in Japan and

those in other areas. Higher values for Japanese were on line
with previous reports [

8

,

9

,

42

,

44

,

47

] and possibly

associated with high dietary Cd intake for years, especially
in the past [

4

].

Age dependency was not evident in the present analysis

both in the exposed and the controls (Table

5

, Fig.

1

).

Previously, Tsuchiya et al. [

44

] observed age-dependent

increase in Cd in kidney cortex up to the age of 60

69 years, probably followed by decrease at higher ages.
Nogawa et al. [

8

] observed age-dependent increase in Cd in

cortex of the non-exposed subjects followed by leveling off
at 50s in men and at 70s in women (two to 17 subjects per
decade of age). According to Lyon et al. [

56

] with the

largest study number of 2,659 cases, Cd in cortex increased
as a function of age from 10 years of age till 40

–50 years

where leveling off took place, followed by a slight decrease
at the ages over 70s. The regression line by Cikrt et al. [

50

]

for Cd in kidney cortex of women appeared to suggest that
the decrease tended to begin earlier in life, e.g., at 40s,
although variation around the line was wide. As the
average ages of people in the present study were 65
(men) to 69 years (women) in the controls and 81 years
(for both sexes) in the exposed (Table

1

), the lack of

age-dependent increase or moderate decreasing trends
should be taken as in a general agreement with forgoing
studies, understanding that the present observation of lack

of age-dependent increase was obtained at the ages when
the age-dependent increase had reached a plateau to
decline at higher ages.

The observation of higher Cd in liver than in kidney

cortex after high Cd exposure (Table

3

) was on line with the

paradox that has been reported since early days [

1

] and

apparently does not agree with the current prevailing
thought in toxicology that toxin will give damage to the
local tissue (e.g., proximal tubules) where it accumulates.
Several possibilities can be postulated for such seemingly
paradoxical findings. For example, dose

–accumulation

relationship may be different after low and high exposure
(e.g., general populations vs. Itai-itai disease patients), most
of Cd that attacked kidney may have leaked out so that the
level at autopsy was low due to cell damage, or
accumulation of Cd to give damage to tubular cells could
be quite topical and high concentration in the tubular cells
would not be detectable (due to dilution with other non-
tubular tissues) when analyzed as cortex. Alternatively,
hepatocytes may be less sensitive (or more tolerable) to Cd
toxicity than tubular cells as Cd in liver may combine with
metallothionein. The mechanism for lower Cd in kidney
cortex in the exposed than in control cases and that for
higher Cd levels in liver than in cortex of the exposed
(Table

3

) apparently need further studies.

Acknowledgments

The authors are grateful to the administration

and staff of Kyoto Industrial Health association for their interest in and
support to this work.

Conflicts of Interest Statement

The authors declare that they have

no conflicts of interest.

Table 5 Cadmium in the kidney and the liver in autopsy cases; comparison of the present results with results reported in literature

Groups

Cd (GM;

μg/g wet tissue)

Kidney

Liver

Cortex

Medulla

Unspecified

No.

e

AV

f

Min

Max

No.

e

AV

f

Min

Max

No.

e

AV

f

Min

Max

No.

e

AV

f

Min

Max

The present study (controls)

a

43

75.6

5.7

206

43

33.7

3.8

107

0

43

7.3

0.8

48.7

5 reports from Japan

b

18

123.3

3.2

139

1

33.5

33.5

33.5

1

42.6

42.6

42.6

4

3.9

2.2

4.5

Reports from other countries

c

All cases

30

19.1

5.7

133

4

9.3

7.7

35.5

37

17.1

0.2

37.1

52

1.3

0.01

7.0

Adults

d

only

27

18.3

5.7

133

4

9.3

7.7

35.5

36

17.1

0.6

37.1

48

1.4

0.4

7.0

a

Cited from Table

2

, except for min and max values

b

[

8

9

,

42

,

44

,

47

]

c

[43, 45

–46, 48–56] (for each report, see the

Appendix

)

d

18 years and over [43, 45

–46, 48–52, 55, 57–59, 61–62, 64–66] (for each report, see the “

Appendix

”)

e

Number of groups studied (number of individuals in the case of the present study)

f

Inverse variance-weighted average (for details of calculation, see the

Statistical Analysis

section) (geometric mean in the case of the present

study)

16

Hayashi et al.

background image

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18

Hayashi et al.

background image

Cadmium

in

the

kidney

and

the

liver

in

autopsy

cases

Y

ear

Authors

Ref.

no.

Location

Methods

Gender

Age

No.

of

cases

Cd

(GM;

μ

g/g

wet

tissue)

Kidney

Liver

Cortex

Medulla

Unsp

’d

GM

GSD

GM

GSD

GM

GSD

GM

GSD

1975

Sumino

et

al.

a

[

42

]

Japan

Flame

AAS

Mixed

Adults

30

42.57

1.10

4.44

1.29

1976

Gross

et

al.

a

[

43

]

USA

Flame

AAS

assumedly

Mixed

19

–24

10

12.24

1.26

0.69

1.20

Mixed

25

–34

10

21.13

1.15

1.07

1.17

Mixed

35

–44

6

26.44

1.12

0.70

1.25

Mixed

45

–54

2

37.14

1.06

1.20

1.46

Mixed

55

–64

9

26.12

1.15

1.63

1.20

Mixed

65+

10

18.02

1.16

1.73

1.14

1976

T

suchiya

et

al.

a

[

44

]

Japan

Flame

AAS

Mixed

0–

9

13

3.25

1.46

Mixed

19

–19

5

24.09

1.38

Mixed

20

–29

38

41.94

1.10

Mixed

30

–39

27

63.73

1.09

Mixed

40

–49

11

74.28

1.15

Mixed

50

–59

6

114.14

1.10

Mixed

60

–69

3

125.09

1.01

Mixed

T

otal

a,g

106

57.74

1.00

1979

Kowal

et

al.

[

45

]

USA

Flame

AAS

Men

19

–19

33

7.57

1.71

0.70

2.23

Men

20

–29

38

13.53

1.66

0.95

1.79

Men

30

–39

33

21.99

1.76

1.21

1.80

Men

40

–49

28

25.83

1.80

1.19

1.88

Men

50

–59

30

25.37

1.68

1.06

2.17

Men

T

otal

162

16.67

1.65

1.00

1.98

1982

Casey

et

al.

a

[

46

]

New

Zealand

Flame

AAS

assumedly

Mixed

Adults

39

–42

132.99

1.25

35.46

1.28

6.95

1.37

1983

Iwao

et

al.

a

[

47

]

Japan

Flame

AAS

Unknown

Smokers

h

24

54.1

1

1.20

4.48

1.17

Unknown

N

on

-s

m

ok

er

s

h

17

36.99

1.23

2.19

1.31

1983

Salmela

et

al.

b

[

48

]

Finland

Flame

AAS

and

GF

AAS

Mixed

0–

9

3

0.17

1.67

0.01

1.470

Mixed

19

–19

16

1.1

1

1.67

0.81

1.470

Mixed

20

–29

24

3.29

1.67

1.44

1.470

Appendix

Cadmium and Other Metal Levels in Autopsy Samples

19

background image

(continued)

Y

ear

Authors

Ref.

no.

Location

Methods

Gender

Age

No.

of

cases

Cd

(GM;

μ

g/g

wet

tissue)

Kidney

Liver

Cortex

Medulla

Unsp

’d

GM

GSD

GM

GSD

GM

GSD

GM

GSD

Mixed

30

–39

12

5.03

1.67

1.43

1.470

Mixed

40

–49

14

4.94

1.67

1.80

1.470

Mixed

50

–59

7

4.75

1.67

1.38

1.470

Mixed

60

–69

4

3.49

1.67

1.95

1.470

Mixed

70+

6

2.62

1.67

1.47

1.470

1986

Nogawa

et

al.

[

8

]

Japan

Flame

AAS

Men

50

–59

13

116.0

1.34

Men

60

–69

14

88.6

1.47

Men

70

–79

13

76.0

1.73

Men

80

–89

4

61.5

2.27

W

omen

50

–59

4

139.0

1.17

W

omen

60

–69

13

113.0

1.41

W

omen

70

–79

8

105.0

1.54

W

omen

80

–89

7

88.9

1.61

1987

Scott

et

al.

b

[

49

]

UK

Flame

AAS

Men

<30

–>90

470

14.7

1.38

7.7

1.26

W

omen

<30

–>90

463

15.8

1.38

7.8

1.26

1990

Cikrt

et

al.

a

[

50

]

Czechoslovakia

Flame

AAS

Men

50

–64

11

1

20.62

1.2

1.06

2.55

Men

65+

101

12.88

1.3

1.20

1.50

W

omen

50

–64

59

22.14

1.4

1.03

2.24

W

omen

65+

147

11.21

1.3

1.38

1.23

1990

Y

oshinaga

et

al.

a

[

9

]

Japan

ICP-AES

Mixed

A

v.

42.5

36,40

62.60

1.28

33.53

1.38

3.56

2.31

1991

T

akács

and

T

atár

a,c

[

51

]

Hungary

GF

AAS

Men

Urban

b

297

10.73

1.29

1.21

1.38

W

omen

Urban

b

234

6.81

1.28

0.89

1.61

Men

Rural

b

287

11.20

1.28

1.19

1.47

W

omen

Rural

b

254

7.42

1.25

0.94

2.00

1995

T

iran

et

al.

d

[

52

]

Austria

GF

AAS

Mixed

25

–36

7

6.38

1.67

0.62

1.470

Mixed

45

–59

7

5.80

1.67

1.51

1.470

Mixed

61

–69

8

10.04

1.67

0.56

1.470

Mixed

70

–79

8

6.72

1.67

0.78

1.470

Mixed

84

–87

4

8.05

1.67

0.79

1.470

1995

T

orra

et

al.

a

[

53

]

Spain

GF

AAS

Mixed

18

–80

50

13.54

1.08

7.69

1.12

0.87

1.12

20

Hayashi et al.

background image

(continued)

Y

ear

Authors

Ref.

no.

Location

Methods

Gender

Age

No.

of

cases

Cd

(GM;

μ

g/g

wet

tissue)

Kidney

Liver

Cortex

Medulla

Unsp

’d

GM

GSD

GM

GSD

GM

GSD

GM

GSD

1998

Orlowski

et

al.

a

[

54

]

Poland

GF

AAS

Mixed

10

–72

39

40.47

1.17

2.17

1.24

1999

Barregård

et

al.

b

[

55

]

Sweden

ICP-MS

Men

30

–39

3

26

1.38

Men

40

–49

6

19

1.38

Men

50

–59

4

9

1.38

Men

60

–69

5

13

1.38

Men

T

otal

18

15

1.38

W

omen

30

–39

2

16

1.38

W

omen

40

–49

3

19

1.38

W

omen

50

–59

6

23

1.38

W

omen

60

–69

6

15

1.38

W

omen

T

otal

17

18

1.38

1999

L

yon

et

al.

d

[

56

]

UK

ICP-MS

Mixed

<10

–90+

2,659

16

1.38

2000

Falnoga

et

al.

a

[

57

]

Slovenia

GF

AAS

Mixed

33

–99

22

5.72

1.49

2001

García

et

al.

a

[

58

]

Spain

ICP-MS

Men

Adults

57

11.84

1.31

1.04

1.18

W

omen

Adults

21

12.73

1.37

0.59

1.30

2002

Y

ilmaz

a

[

59

]

T

urkey

GF

AAS

Mixed

11

–30

14

0.61

1.20

0.44

1.34

Mixed

31

–50

18

0.79

1.1

1

0.57

1.12

Mixed

51+

11

0.80

1.19

0.57

1.18

2002

Satarug

et

al.

a

[

60

]

Australia

ICP-MS

Mixed

1–

60+

61

11.43

1.35

0.72

1.32

2002

L

yon

et

al.

[

61

]

UK

ICP-MS

Mixed

<6+

147

0.03

1.47

2004

Lalor

et

al.

a

[

62

]

Jamaica

Flame

AAS

and

GF

AAS

Men

40+

21

31.04

1.17

2.30

1.48

W

omen

40+

18

43.98

1.20

5.52

1.38

2005

Bocio

et

al.

e

[

63

]

Spain

ICP-MS

Mixed

Unknown

22

14.32

1.38

1.02

1.47

2006

Johansen

et

al.

a

[

64

]

Greenland

GF

AAS

Mixed

19

–29

5–

9

10.70

1.15

1.12

1.29

Mixed

30

–39

8

17.30

1.03

1.88

1.04

Mixed

40

–49

7–

10

21.77

1.03

1.26

1.36

Mixed

50

–59

14

–16

14.93

1.23

1.61

1.14

Mixed

60

–69

16

–17

13.65

1.16

1.24

1.31

Mixed

70

–79

18

–26

13.74

1.12

2.15

1.22

Mixed

80

–89

6

4.17

1.24

1.30

1.25

Cadmium and Other Metal Levels in Autopsy Samples

21

background image

(continued)

Y

ear

Authors

Ref.

no.

Location

Methods

Gender

Age

No.

of

cases

Cd

(GM;

μ

g/g

wet

tissue)

Kidney

Liver

Cortex

Medulla

Unsp

’d

GM

GSD

GM

GSD

GM

GSD

GM

GSD

Mixed

T

otal

71

–91

13.82

1.16

1.59

1.24

2010

Schöpfer

et

al.

[

65

]

Germany

GF

AAS

Men

Smokers

h

129

(smokers

+

non-smokers)

27.0

1.668

Men

N

on

-s

m

ok

er

s

h

7.1

1.668

2010

Barregård

et

al.

f

[

66

]

Sweden

ICP-MS

Mixed

Smokers

h

68

16.7

1.668

Mixed

N

on

-s

m

ok

er

s

h

41

8.30

1.668

Year

year

of

publication,

Flame

AAS

flame

atomic

absorption

spectrometry

,

GF

AAS

graphite

furnace

atomic

absorption

spectrometry

,

ICP-MS

inductively

coupled

mass

spectrometry

,

ICP-AES

inductively

coupled

atomic

emission

spectrometry

,

Mixed

men

and

women

in

combination,

Unsp.

’d

unspecified

with

regard

to

cortex

or

medulla

a

GM

and

GSD

are

estimated

from

AM

and

ASD

by

the

moment

method

(Sugita

and

T

suchiya

[

32

])

b

Originally

only

GM

values

are

given;

GSD

is

estimated

as

a

grand

average

of

GSD

of

38,

3,

22,

and

4

cases

for

cortex,

medulla,

kidney

unspecified,

and

live

r,

respectively

c

Age

unknown

d

Originally

only

medians

are

given;

GSD

is

estimated

as

described

in

footnote

“b

e

Only

AM

is

given

(with

no

ASD).

GM

is

estimated

as

81%

and

75%

of

the

reported

AM;

the

81%

and

75%

are

the

average

GM/AM

ratios

of

other

24

and

37

cases

for

cort

ex

and

liver

,

respectively

f

Biopsy

samples

g

Including

three

cases

of

>70-years-old

subjects

h

Adults

22

Hayashi et al.


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