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UROLOGICAL CANCERS IN
WA L ES
(DIAGNOSIS PERIOD 1995-2004)
Occasional report S0602
Welsh Cancer Intelligence
and Surveillance Unit
1
TABLE OF CONTENTS
Introduction
2
Local Health Boards in Wales
3
Incidence of Urological Cancers in Wales, 1995-2004
4
Mortality of Urological Cancers in Wales, 1995-2004
10
Risk Factors and Aetiology of Urological Cancers
15
Health Statistics Wales
19
References
21
INTRODUCTION
The following occasional report examines trends in incidence and mortality of
urological cancers in Wales for the ten year period 1995-2004.
Total numbers of cases are explored along with European Age Standardised
Rates (EASR) per 100,000 population in Wales and by Local Health Board (LHB)
in Wales to determine the variability of incidence and mortality rates throughout
Wales. The EASR adjusts crude rates to take in effect the differing age structure
that exists between the Welsh population and the European population. Thus
direct comparisons between Welsh rates and European rates can be examined.
For UK comparisons and review of risk factors we have extracted some figures
and text from the UK and Ireland Cancer Atlas. WCISU contributed data and text
to this collaborative UK project.
2
Figure A shows the LHBs in Wales that the following report examines.
Figure A: Local Health Boards in Wales.
NORTH WALES CANCER NETWORK
Code
Local Health Board
NA
Anglesey
NC
Gwynedd
NE
Conwy
NG
Denbighshire
NJ
Flintshire
NL
Wrexham
NA
NJ
NE
NG
NL
NC
SOUTH WEST WALES CANCER NETWORK
Code
Local Health Board
NN
Powys
NQ
Ceredigion
NS
Pembrokeshire
NU
Carmarthenshire
NX
Swansea
NZ
Neath & Port Talbot
NN
NQ
NS
NU
PL
PP
PH
NZ
PF
NX
PM
PK
PR
PB
PT
PD
3
SOUTH EAST WALES CANCER NETWORK
Code
Local Health Board
PB
Bridgend
PD
Vale of Glamorgan
PF
Rhondda Cynon Taff
PH
Merthyr Tydfil
PK
Caerphilly
PL
Blaenau Gwent
PM
Torfaen
PP
Monmouthshire
PR
Newport
PT
Cardiff
INCIDENCE OF UROLOGICAL CANCERS IN WALES 1995-2004
Urological Cancer can be split into various site specific cancers those being:
•
•
•
•
•
Prostate Cancer (ICD 10 code C61)
Testicular Cancer (ICD 10 code C62)
Penile Cancer (ICD 10 code C60)
Bladder Cancer (ICD10 code C67)
Kidney Cancer (ICD10 code C64-C66)
Table 1 shows the total number of cases for urological cancers in Wales for the ten-year
period 1995-2004.
Table 1: Number of cases registered in Wales with urological cancers for the
period 1995-2004.
Male
Prostate (males only)
Testis (males only)
Penis (males only)
Bladder
Kidney
1995
1996
1997
1998
1999
2000
2001
2002
2003
2004
1253
110
30
575
195
1262
97
34
634
198
1320
81
16
594
219
1298
92
23
604
190
1570
72
21
641
243
1655
75
25
637
219
1774
81
18
661
250
1807
87
19
604
239
2003
112
20
636
227
2281
94
21
671
267
1995
1996
1997
1998
1999
2000
2001
2002
2003
2004
225
119
228
105
229
132
238
144
252
150
262
139
244
133
247
156
246
161
252
163
1995
1996
1997
1998
1999
2000
2001
2002
2003
2004
1253
110
30
800
314
1262
97
34
862
303
1320
81
16
823
351
1298
92
23
842
334
1570
72
21
893
393
1655
75
25
899
358
1774
81
18
905
383
1807
87
19
851
395
2003
112
20
882
388
2281
94
21
923
430
Female
Prostate (males only)
Testis (males only)
Penis (males only)
Bladder
Kidney
Person
Prostate (males only)
Testis (males only)
Penis (males only)
Bladder
Kidney
Prostate cancer was the most common cancer in males for the ten year diagnosis period
1995-2004. This cancer accounted for approximately 21% of all male malignancies
(excluding non-melanoma skin cancer). There were on average 1622 cases of prostate
cancer per year for the period 1995-2004. Table 1 shows a general increase in prostate
cancer incidence over the ten-year period 1995-2004 – this is attributed to Prostate
4
Specific Antigen (PSA) testing – cases are being diagnosed earlier than what they would
have had it not been for PSA testing.
There was a slight decrease in testicular cancer incidence in the late 1990s but have
steadily increased throughout the early 2000s back to its mid 1990s level. Incidence
figures for penile cancer steadily decreases throughout the ten year period investigated.
Incidence of penile cancer is very rare and approximately 23 cases are diagnosed per
year in Wales.
Bladder cancer incidence figures continue to rise for both sexes for the period 19952004 (17% higher in 2004 compared with 1995 for males and 12% higher for females).
Kidney cancer follows a similar trend as bladder cancer with a general increase in
incidence for both sexes throughout the ten year period.
Figure 1 shows the European Age Standardised Rate (EASR) per 100,000 population
for three year rolling averages for urological cancers in males in Wales for the period
1995-2004.
Figure 1: EASR per 100,000 population: three year rolling averages for male
urological cancers in Wales 1995-2004.
120
100
80
60
40
20
0
1995-1997
1996-1998
1997-1999
Prostate
1998-2000
1999-2001
Testis
Penis
Bladder
2000-2002
2001-2003
2002-2004
Kidney
The EASR takes into account the differing age structure in Wales compared with the
European population. Figure 1 shows EASR for testis, penis, bladder and kidney are
stable over the ten-year period whereas for prostate cancer there is a sharp increase in
the EASR from approximately 70 per 100,000 population for 1995-1997 to approximately
110 per 100,000 population for 2002-2004.
Figure 2 shows the trend in EASR per 100,000 population for female bladder and kidney
cancer in Wales for the period 1995-2004.
5
Figure 2: EASR per 100,000 population: three year rolling averages for female
urological cancers in Wales 1995-2004.
14
12
10
8
6
4
2
0
1995-1997
1996-1998
1997-1999
1998-2000
1999-2001
Bladder
2000-2002
2001-2003
2002-2004
Kidney
Figure 2 shows a slight increase in EASR per 100,000 population for bladder cancer in
the late 1990s/early 2000s before falling back to its mid 1990s levels. Female kidney
cancer shows a general increase in EASR per 100,000 population for three year rolling
averages for the period 1995-2004.
Table 2 shows the number of male and female urological cancers for the ten year period
1995-2004 for all twenty two Local Health Boards (LHB) in Wales along with 95%
confidence intervals. Penile cancer is not shown due to the very small numbers of
cases.
6
Table 2: Total numbers of cases registered with urological cancers by Local
Health Board in Wales, 1995-2004.
Male
Total
*Prostate (males)
95% CI
EASR
Total
*Testis (males)
EASR
95% CI
Total
Bladder
EASR
95% CI
Total
Kidney
EASR
95% CI
Isle of Anglesey
Gwynedd
Conwy
Denbighshire
Flintshire
Wrexham
Powys
Ceredigion
Pembrokeshire
Carmarthenshire
Swansea
Neath Port Talbot
Bridgend
The Vale of Glamorgan
Cardiff
Rhondda Cynon Taff
Merthyr Tydfil
Caerphilly
Blaenau Gwent
Torfaen
Monmouthshire
Newport
393
688
922
686
787
682
853
408
751
1104
1423
695
680
696
1535
1151
234
670
378
378
524
585
81.3
85.1
101.1
100.3
93.5
90.2
88.3
75.6
93.7
87.9
96.0
77.2
86.7
94.4
96.1
84.9
70.8
71.7
85.0
70.5
89.4
73.4
(73.1,89.4)
(78.7,91.6)
(94.3,107.8)
(92.6,108.0)
(87.0,100.1)
(83.4,97.1)
(82.3,94.3)
(68.1,83.0)
(86.9,100.5)
(82.6,93.1)
(90.9,101.1)
(71.4,83.1)
(80.1,93.4)
(87.3,101.5)
(91.2,101.0)
(79.9,90.0)
(61.6,80.1)
(66.2,77.2)
(76.3,93.8)
(63.2,77.7)
(81.7,97.1)
(67.4,79.5)
17
30
27
36
50
45
43
26
35
62
77
48
41
49
87
65
14
36
17
26
20
50
5.2
5.5
5.8
8.6
6.9
7.1
7.3
8.1
7.1
8.0
7.2
7.5
6.5
9.4
5.6
5.8
5.3
4.4
5.2
6.2
5.2
7.5
(2.7,7.7)
(3.5,7.5)
(3.6,8.1)
(5.7,11.4)
(5.0,8.8)
(5.0,9.1)
(5.1,9.5)
(4.9,11.2)
(4.7,9.5)
(6.0,10.1)
(5.6,8.8)
(5.3,9.6)
(4.5,8.5)
(6.8,12.1)
(4.4,6.7)
(4.4,7.3)
(2.5,8.1)
(3.0,5.9)
(2.7,7.7)
(3.8,8.6)
(2.9,7.5)
(5.4,9.6)
153
263
303
240
333
274
262
155
251
452
511
305
251
261
572
434
112
308
127
179
187
324
32.6
34.7
35.2
35.8
40.1
36.9
28.0
30.4
32.5
37.3
35.2
35.0
32.8
36.0
35.9
32.7
34.8
33.2
30.4
32.8
34.2
41.8
(27.4,37.9)
(30.5,39.0)
(31.0,39.4)
(31.1,40.4)
(35.8,44.5)
(32.5,41.4)
(24.5,31.5)
(25.5,35.3)
(28.4,36.6)
(33.8,40.8)
(32.1,38.4)
(31.0,39.0)
(28.7,36.9)
(31.6,40.4)
(32.9,38.9)
(29.6,35.9)
(28.3,41.3)
(29.4,37.0)
(25.0,35.8)
(27.9,37.7)
(29.3,39.2)
(37.2,46.4)
58
103
111
79
114
92
115
44
106
173
192
113
97
93
188
164
36
96
56
56
65
96
12.8
14.6
14.5
12.5
14.1
13.2
13.7
9.4
14.8
15.5
14.6
14.0
13.1
13.6
12.1
12.8
11.6
10.7
14.1
11.1
12.3
12.8
(9.4,16.1)
(11.7,17.5)
(11.7,17.3)
(9.7,15.4)
(11.5,16.8)
(10.5,15.9)
(11.1,16.3)
(6.6,12.2)
(11.9,17.7)
(13.2,17.9)
(12.5,16.7)
(11.4,16.7)
(10.5,15.8)
(10.8,16.4)
(10.4,13.9)
(10.8,14.8)
(7.7,15.4)
(8.6,12.9)
(10.3,17.8)
(8.2,14.1)
(9.3,15.3)
(10.2,15.4)
Wales
16223
87.4
(86.0,88.8)
901
6.5
(6.1,7.0)
6257
34.7
(33.8,35.6)
2247
13.3
(12.7,13.8)
Female
Total
Bladder
EASR
95% CI
Total
Kidney
EASR
95% CI
Isle of Anglesey
Gwynedd
Conwy
Denbighshire
Flintshire
Wrexham
Powys
Ceredigion
Pembrokeshire
Carmarthenshire
Swansea
Neath Port Talbot
Bridgend
The Vale of Glamorgan
Cardiff
Rhondda Cynon Taff
Merthyr Tydfil
Caerphilly
Blaenau Gwent
Torfaen
Monmouthshire
Newport
62
107
126
91
108
112
96
53
96
170
173
145
103
110
220
199
44
116
54
75
77
86
11.0
10.1
10.8
9.3
9.8
10.9
8.1
7.3
9.5
10.5
9.4
12.0
9.7
11.5
10.1
11.0
10.4
9.4
9.0
10.7
10.6
7.4
(8.1,14.0)
(8.0,12.2)
(8.6,12.9)
(7.1,11.5)
(7.9,11.8)
(8.7,13.1)
(6.3,9.9)
(5.1,9.4)
(7.5,11.6)
(8.8,12.2)
(7.9,11.0)
(9.9,14.2)
(7.7,11.7)
(9.2,13.8)
(8.6,11.5)
(9.4,12.7)
(7.1,13.7)
(7.6,11.2)
(6.3,11.6)
(8.1,13.2)
(8.0,13.2)
(5.7,9.2)
31
61
67
47
58
61
64
30
64
84
108
80
53
69
132
117
31
66
30
42
46
61
5.7
6.7
7.4
6.0
5.9
6.5
6.6
5.1
7.1
5.9
6.8
7.7
5.6
8.7
7.4
7.3
7.7
5.9
5.9
6.6
7.6
6.4
(3.5,7.9)
(4.9,8.6)
(5.4,9.3)
(4.1,8.0)
(4.3,7.5)
(4.8,8.3)
(4.9,8.3)
(3.0,7.2)
(5.2,9.0)
(4.5,7.2)
(5.4,8.2)
(5.8,9.5)
(4.0,7.2)
(6.5,10.8)
(6.1,8.8)
(5.9,8.7)
(4.8,10.6)
(4.4,7.4)
(3.7,8.2)
(4.5,8.7)
(5.3,9.9)
(4.7,8.1)
Wales
2423
10.0
(9.5,10.4)
1402
6.7
(6.3,7.1)
It can be seen that LHBs in North Wales have the highest EASR per 100,000 population
for prostate cancer compared with Wales as a whole (significantly higher in Conwy and
Denbighshire). Note that penile cancer by LHB is not presented here due to the very
small numbers observed by LHB in Wales. The highest rates of testicular cancer are
located in the Vale of Glamorgan whereas the lowest rates of testicular cancer are
located in the Isle of Anglesey and Monmouthshire. EASR per 100,000 population for
male bladder cancer range from 28.0 per 100,000 population in Powys (significantly
lower compared with Wales) to 41.8 per 100,000 population in Newport (significantly
higher compared with Wales). EASR per 100,000 population for male kidney cancer
vary throughout Wales.
7
EASR per 100,000 population for female bladder cancer and kidney cancer vary
throughout Wales but are high in the Vale of Glamorgan for both cancers and low in
Ceredigion for both cancers (significantly lower for bladder cancer).
The following information was taken from the “Cancer Atlas of the UK and Ireland 19912000”. The report is available electronically by clicking on the above link.
Figure 3 shows EASR per 100,000 population for each country and region of England in
the UK and Ireland for the period 1991-1999 for prostate cancer.
Figure 3: EASR per 100,000 population for prostate cancer by country and region
of England in the UK and Ireland 1991-1999.
Figure 3 shows that rates in Wales appear slightly higher than the UK and Ireland
average although Ireland has the highest EASR per 100,000 population for prostate
cancer.
Figure 4 shows the standardised incidence ratio for testicular cancer by health authority
in UK and Ireland 1991-1999.
8
Figure 4: Standardised incidence ratio for testicular cancer by health authority in
UK and Ireland 1991-1999.
* Ratio of directly age standardised rate in health authority to UK and Ireland average
Figure 4 shows lower than expected rates in South Wales and higher than expected
rates in North Wales. Scotland has the highest testicular rates.
9
MORTALITY OF UROLOGICAL CANCERS IN WALES 1995-2004
Table 3 shows the total number of deaths for various urological cancers for the ten year
period 1995-2004 in Wales.
Table 3: Total number of deaths for urological cancers in Wales for the period
1995-2004.
Male
Prostate (males only)
Testis (males only)
Penis (males only)
Bladder
Kidney
1995
1996
1997
1998
1999
2000
2001
2002
2003
2004
593
6
8
166
83
513
12
7
167
103
534
4
9
187
94
497
4
7
181
107
479
0
3
128
117
498
6
7
152
93
616
2
7
174
111
529
3
5
152
121
579
4
2
167
111
633
6
2
150
118
1995
1996
1997
1998
1999
2000
2001
2002
2003
2004
93
60
114
53
65
56
81
65
84
67
84
72
77
60
103
67
86
74
83
71
1995
1996
1997
1998
1999
2000
2001
2002
2003
2004
593
6
8
259
143
513
12
7
281
156
534
4
9
252
150
497
4
7
262
172
479
0
3
212
184
498
6
7
236
165
616
2
7
251
171
529
3
5
255
188
579
4
2
253
185
633
6
2
233
189
Female
Prostate (males only)
Testis (males only)
Penis (males only)
Bladder
Kidney
Person
Prostate (males only)
Testis (males only)
Penis (males only)
Bladder
Kidney
There are a very small number of deaths for testicular and penile cancer in Wales. The
number of prostate cancer deaths initially fell by 19% from 1995 to 1999 but has
increased from 2000 onwards. The numbers of male bladder cancer has remained
stable whereas the numbers of deaths for male kidney cancer has increased over the
ten year period. A similar trend is seen for female bladder and kidney cancer.
Figure 5 shows the EASR per 100,000 population in Wales for three year rolling
averages for mortality of male urological cancers for the period 1995-2004 and figure 6
shows the EASR per 100,000 population in Wales for three year rolling averages for
mortality of female bladder and kidney cancer for the period 1995-2004.
10
Figure 5: EASR per 100,000 population: three year rolling averages for mortality of
male urological cancers in Wales 1995-2004.
35
30
25
20
15
10
5
0
1995-1997
1996-1998
1997-1999
Prostate
1998-2000
1999-2001
Testis
Penis
Bladder
2000-2002
2001-2003
2002-2004
Kidney
Figure 6: EASR per 100,000 population: three year rolling averages for mortality of
female urological cancers in Wales 1995-2004.
4
3.5
3
2.5
2
1.5
1
0.5
0
1995-1997
1996-1998
1997-1999
1998-2000
Bladder
11
1999-2001
Kidney
2000-2002
2001-2003
2002-2004
EASR per 100,000 population in Wales are constant for mortality of testicular cancer and
penile cancer. EASR for bladder cancer and kidney cancer are stable for males
whereas for prostate cancer there is a decrease for the first four periods followed by an
increase for the later periods.
For female urological cancers an increase in EASR per 100,000 population for kidney
cancer is followed by a decrease in EASR per 100,000 population for bladder cancer
and vice versa. This can also be seen in males (but not so clear due to the scale used).
Table 4 shows the total number of deaths and EASR per 100,000 population by LHB in
Wales for the period 1995-2004. Penile cancer and testicular cancer figures are not
shown here due to the very small number of deaths in Wales for this period.
Table 4: Total numbers of deaths for urological cancers by Local Health Board in
Wales, 1995-2004.
Male
*Prostate (males)
Total EASR
95% CI
*Testis (males)
Total EASR 95% CI
Total
Bladder
EASR 95% CI
Total
Kidney
EASR 95% CI
Isle of Anglesey
Gwynedd
Conwy
Denbighshire
Flintshire
Wrexham
Powys
Ceredigion
Pembrokeshire
Carmarthenshire
Swansea
Neath Port Talbot
Bridgend
The Vale of Glamorgan
Cardiff
Rhondda Cynon Taff
Merthyr Tydfil
Caerphilly
Blaenau Gwent
Torfaen
Monmouthshire
Newport
138
259
276
216
200
212
291
147
308
363
434
242
239
222
481
407
88
272
144
126
175
231
28.4
31.9
28.0
28.5
23.5
27.5
28.4
26.0
38.9
28.5
28.1
26.5
29.6
29.1
27.6
30.7
25.8
29.8
34.4
23.9
29.2
28.7
(23.6,33.2)
(28.0,35.8)
(24.6,31.4)
(24.6,32.4)
(20.2,26.8)
(23.8,31.3)
(25.1,31.7)
(21.7,30.3)
(34.5,43.3)
(25.5,31.5)
(25.4,30.8)
(23.0,29.9)
(25.8,33.5)
(25.2,33.0)
(25.0,30.1)
(27.6,33.8)
(20.3,31.3)
(26.1,33.4)
(28.6,40.1)
(19.6,28.2)
(24.8,33.6)
(24.9,32.5)
3
0
2
3
2
1
1
0
1
3
6
2
2
1
3
1
1
6
1
4
0
4
0.9
0.0
0.4
0.5
0.3
0.1
0.1
0.0
0.2
0.3
0.6
0.3
0.3
0.2
0.2
0.1
0.3
0.7
0.4
0.9
0.0
0.6
(0.0,1.8)
(0.0,0.0)
(0.0,1.0)
(0.0,1.0)
(0.0,0.6)
(0.0,0.3)
(0.0,0.2)
(0.0,0.0)
(0.0,0.5)
(0.0,0.8)
(0.1,1.0)
(0.0,0.7)
(0.0,0.7)
(0.0,0.5)
(0.0,0.4)
(0.0,0.3)
(0.0,1.0)
(0.1,1.2)
(0.0,1.1)
(0.0,1.8)
(0.0,0.0)
(0.0,1.2)
24
68
70
63
75
69
91
33
80
119
105
84
76
61
151
111
32
87
38
55
51
81
4.6
8.8
7.5
8.6
9.0
9.0
9.3
5.5
9.8
9.4
7.0
9.1
9.4
8.2
8.9
8.3
9.3
9.5
9.0
9.7
9.2
9.9
(2.7,6.5)
(6.6,10.9)
(5.6,9.3)
(6.4,10.7)
(7.0,11.1)
(6.8,11.1)
(7.3,11.2)
(3.6,7.4)
(7.6,12.0)
(7.6,11.1)
(5.6,8.4)
(7.1,11.2)
(7.2,11.6)
(6.1,10.3)
(7.4,10.3)
(6.7,9.9)
(6.0,12.6)
(7.4,11.5)
(6.1,12.0)
(7.1,12.3)
(6.6,11.7)
(7.7,12.1)
23
39
64
37
58
41
51
23
47
85
91
54
49
38
78
71
24
51
31
20
35
48
5.2
5.2
8.2
5.6
7.0
5.9
6.1
4.5
6.6
7.3
6.8
6.6
6.8
5.2
4.9
5.5
7.6
5.5
7.8
3.8
6.4
6.1
(3.1,7.4)
(3.6,6.9)
(6.1,10.3)
(3.8,7.5)
(5.2,8.9)
(4.1,7.7)
(4.4,7.9)
(2.6,6.4)
(4.7,8.6)
(5.7,8.9)
(5.4,8.2)
(4.8,8.3)
(4.8,8.7)
(3.5,6.9)
(3.8,6.0)
(4.2,6.8)
(4.5,10.8)
(4.0,7.0)
(5.0,10.5)
(2.1,5.5)
(4.2,8.5)
(4.3,7.8)
Wales
5471
28.8
(28.0,29.5)
47
0.3
(0.2,0.4)
1624
8.6
(8.2,9.0)
1058
6.1
(5.7,6.5)
Total
Kidney
EASR 95% CI
Female
Total
Bladder
EASR
95% CI
Isle of Anglesey
Gwynedd
Conwy
Denbighshire
Flintshire
Wrexham
Powys
Ceredigion
Pembrokeshire
Carmarthenshire
Swansea
Neath Port Talbot
Bridgend
The Vale of Glamorgan
Cardiff
Rhondda Cynon Taff
Merthyr Tydfil
Caerphilly
Blaenau Gwent
Torfaen
Monmouthshire
Newport
17
35
44
32
39
46
36
26
34
53
51
57
48
31
70
71
16
37
24
33
32
38
2.5
2.6
2.9
2.6
3.2
3.7
2.3
3.4
2.6
2.6
2.1
3.8
3.9
2.6
2.6
3.4
2.8
2.7
3.6
3.7
3.6
2.8
(1.2,3.8)
(1.7,3.6)
(1.9,3.9)
(1.6,3.6)
(2.1,4.2)
(2.5,4.8)
(1.5,3.1)
(2.0,4.9)
(1.7,3.6)
(1.9,3.4)
(1.5,2.7)
(2.7,4.8)
(2.7,5.1)
(1.6,3.6)
(1.9,3.2)
(2.5,4.2)
(1.4,4.2)
(1.8,3.6)
(2.0,5.2)
(2.4,5.1)
(2.3,5.0)
(1.8,3.7)
13
30
36
18
22
39
36
13
29
41
37
29
27
26
59
60
13
34
21
18
15
29
1.9
2.9
3.1
1.6
2.0
3.9
3.0
1.8
2.8
2.4
1.8
2.3
2.5
2.9
3.1
3.4
3.1
2.8
3.7
2.2
1.8
2.9
(0.8,3.0)
(1.8,4.1)
(2.0,4.3)
(0.7,2.5)
(1.1,2.9)
(2.6,5.3)
(1.9,4.1)
(0.7,2.9)
(1.7,3.9)
(1.6,3.2)
(1.2,2.4)
(1.4,3.2)
(1.5,3.5)
(1.7,4.1)
(2.2,3.9)
(2.5,4.3)
(1.3,4.9)
(1.8,3.8)
(2.0,5.5)
(1.1,3.2)
(0.9,2.8)
(1.8,4.0)
Wales
870
2.9
(2.7,3.1)
645
2.7
(2.4,2.9)
12
Gwynedd has the highest EASR per 100,000 population in Wales at 31.9 per 100,000
population for prostate cancer and Flintshire has the lowest EASR (significant compared
with Wales) per 100,000 population. Southern areas of Wales tend to have the highest
EASR per 100,000 population for bladder cancer. Note that where the total number of
deaths for a LHB is small, an increase of just one or two cases can dramatically affect
the EASR per 100,000 population.
The following information has been taken from the “Cancer Atlas of the UK and Ireland
1991-2000”.
Figure 7 shows the EASR per 100,000 population for mortality of male and female
bladder cancer by country in the UK and Ireland and region of England for the period
1991-2000.
Figure 7: EASR per 100,000 population for bladder cancer by country and region
of England in the UK and Ireland 1991-2000.
The EASR per 100,000 population is lower in Wales than the UK and Ireland average for
both males and females. The highest rates are located in Scotland whereas the lowest
rates are located in Ireland for both sexes.
Figure 8 show the standardised mortality ratios by health authority in the UK and Ireland
for prostate cancer and testicular cancer for the period 1991-2000.
13
Figure 8: Standardised mortality ratios by health authority in UK and Ireland 19912000.
Prostate cancer
Testicular cancer
* Ratio of directly age standardised rate in health authority to UK and Ireland average
The map for prostate cancer generally shows similar ratios throughout the UK and
Ireland whereas the mortality ratios for testicular cancer show greater variation
throughout the UK and Ireland. Mortality ratios of testicular cancer are higher in parts of
Wales compared with other health authorities but the highest mortality ratios are found in
parts of Ireland and Scotland.
14
RISK FACTORS AND AETIOLOGY OF UROLOGICAL CANCERS
(Text taken from the Cancer Atlas of the UK and Ireland)
PROSATE CANCER
The aetiology of prostate cancer is not well known. Despite evidence of important
variations in incidence from international comparisons and studies of migrants, specific
causal factors (such as environmental, life-style, diet, and occupation) have not been
identified conclusively. An area of current research is diet and obesity.2,3 In the past,
many studies have explored reproductive characteristics and sexual habits, including
frequency of intercourse and masturbation, but with inconsistent results.4
It is clear that black men have higher incidence than white men. In the SEER Program of
the United States National Cancer Institute, the age-standardised incidence in black men
is about 70 per cent higher than in white men.1 In the UK, the largest concentrations of
black people are in London and particularly in Lambeth, Southwark and Lewisham (19
per cent); and East London and the City (14 per cent). Neither these areas, nor London
as a whole, appear to have particularly high incidence rates of prostate cancer (Map
20.2).
Consistent with the relatively high incidence in Ireland observed in this study, a study of
Irish migrants found increased incidence in Irish men living in the UK.5
The main difficulty with aetiological research in prostate cancer is the heterogeneity of
the disease, ranging from highly prevalent but clinically indolent cancers, to highly
aggressive and often fatal disease.6 Any assessment of incidence or survival will be
highly sensitive to the intensity of diagnostic procedures in the community (for example,
through testing for PSA) and to temporal and spatial variation in the use of such
procedures. The mortality rate is much less influenced by such changes. In research into
possible causes of prostate cancer it is imperative that asymptomatic, PSA-detected
disease is considered separately from symptomatic disease, as the risk factors could be
different. Because of these issues, it may be preferable to use prostate cancer mortality
as an endpoint, even in research into possible causes.
TESTICULAR CANCER
There is a considerable body of evidence, both indirect and direct, which indicates that
the rate-limiting steps in the development of testicular cancer occur very early in life,
most probably early in gestation around the time of differentiation of the genital
organs.7,8-11 The susceptible cell population from which testicular germ cell cancers arise
are most likely the primordial germ cells, which in normal development differentiate into
spermatogonia in males or oocytes in females. Occasionally, primordial germ cells
persist in the undifferentiated state and give rise to a pre-malignant condition known as
testicular carcinoma in situ, which in turn has a very high probability of progression to
invasive cancer after the onset of puberty.12
Consistent risk factors for testicular cancer are congenital malformations of the genital
organs (particularly cryptorchidism – failure of the testicles to descend into the scrotum),
low birth weight and intrauterine growth retardation, low maternal parity, and subfertility.13-15 Other postulated risk factors include maternal exposure to exogenous
15
oestrogens during the first trimester of pregnancy, and a history of trauma to the affected
testicle.16 It has been suggested that heritability plays a role in the aetiology of testicular
cancer, with a family history of testicular cancer among first degree relatives being a
postulated risk factor.16 It has been estimated that the risk of testicular cancer in the
brothers of cases is 2.2 per cent.17
Rates of testicular cancer vary between different ethnic groups and different European
populations, with higher rates in males of European origin than Asian and black males.18
The incidence in England and Wales is amongst the highest in the world.19 In the SEER
cancer registries of the United States National Cancer Institute, the age-standardised
incidence rate is five times higher in white males than in black males. In Los Angeles,
where incidence rates are reported separately by ethnic group, the rates are: nonHispanic white 5.7 per 100,000; Hispanic white 3.1; Japanese 2.3; black 1.4; Chinese
1.0; Filipinos 0.8; and Koreans 0.6. Rates around 1.0 per 100,000 or lower are reported
from China, India and Pakistan.
BLADDER CANCER
Substantial epidemiological evidence supports a relationship between bladder cancer
and cigarette smoking. It has been suggested that up to 40 per cent of all male and 10
per cent of female cases might be ascribable to this exposure.20 The relative risks are
around 2-3 fold.21 The causative links were established as the result of positive
associations from at least 8 cohort and over 15 case-control studies, the best known
cohort study being that of British doctors.22 The striking consistency of their findings, the
dose-response relationships23,24 and the identification of at least two known bladder
carcinogens in cigarette smoke (2-naphthylamine and 4-aminobiphenyl) as well as the
identification of aromatic amine based DNAadducts, 25 all give confidence that there is a
causative link. However, there are only weak overall correlations in incidence between
the sexes and very little agreement with the geographical pattern of lung cancer in the
UK and Ireland or with long-term trends in lung cancer in either sex. The geographical
distribution of bladder cancer, despite the links with cigarette smoking, does not show a
marked association with areas of higher tobacco consumption, as does that for lung
cancer. This seems to indicate that cigarette smoking is not a dominant factor in the
aetiology of the condition and raises the possibility that the associations with smoking
may be confounded with other factors. The relative risks found in some studies may be
related to the kind of tobacco smoked. Black tobacco (composed of air-cured tobacco)
used more in southern Europe produces more 4- aminobiphenyl in the mainstream
smoke than blond (fluecured) tobacco.26,27 The risk of bladder cancer is 2 to 3 times
higher among smokers of black tobacco than among smokers of blond tobacco.28
Bladder cancer is strongly linked to occupational and environmental exposure to
chemicals. Occupational exposure is estimated to be the cause of around 20 per cent of
current bladder cancer cases. Studies in the dye intermediates industry and the rubber
industry in the 1950s have indicated that arylamines such as 2-napthylamine, benzidine
and (in the USA) 4-aminobiphenyl are all human bladder carcinogens.29,30 Consequently,
the industrial use of 2-napthylamine and of benzidine was banned in the UK in 1950 and
1962, respectively. However, deaths from occupational cancer may take place several
decades after initial causal exposures. Long latent periods of up to 40 years or more
from first industrial exposure are observed and therefore, despite removal of known
carcinogens, occupationally caused bladder cancers may continue to be diagnosed and
account for the excess bladder mortality that occurs to workers in the chemical industry.
16
Also, recent studies still show excess risk of bladder cancer in workers of the rubber
industry with no recorded exposure to 2-napthylamine. This indicates that other agents
in this industry may be associated with the occurrence of bladder cancer among rubber
workers.31
The source of other possible chemical carcinogens causing bladder cancer is more
controversial, being based largely on case-control studies only. It is possible that leather
workers,32 painters,33,34 truck drivers,35 aluminium workers,36 and those in jobs with a
high exposure to printing inks, cutting oils and solder37 all might be at some slight excess
risk of bladder cancer. The risk areas for females had a higher percentage of workers in
textile-related occupations.38 High-risk areas had more male glass workers and female
ceramic workers than the national average.38 Investigation of excess bladder cancer
mortality for the period 1968-78 in London using death certificate data showed significant
rate ratios for all road transport drivers and leather workers.39 It is possible therefore,
that the observed regional variation in bladder cancer incidence and mortality could in
part be a reflection of a number of different occupational exposures from industries
concentrated in different areas of the UK and Ireland.
Some treatments for cancer have been attributed to increasing the risk of subsequent
bladder cancer. The alkylating agent cyclophosphamide used largely in cancer
chemotherapy confers a risk of bladder cancer.40 Ionising irradiation undoubtedly can
cause bladder cancer in people heavily exposed, such as those treated for cervix cancer
by external beam radiation.41 However, this risk cannot provide a geographical
explanation of bladder cancer patterns, as these risks apply only to a welldefined and
small group of people.
Environmental studies show increasing evidence that arsenic ingestion causes a risk of
bladder cancer. Documented causes are exposure to high levels of arsenic in the
national environment as occurred in Taiwan,42 or (unusual) arsenic ingestion of Fowler’s
solution as a medication.43 Chlorination of drinking water has been linked to a modestly
increased risk of bladder cancer in the USA44 but the levels of chlorination in the British
Isles are low (well within World Health Organisation guidelines) and generally uniform in
those houses supplied with mains water. However, the excessive use of phenacetin
(acetaminophen) confers a risk of cancer to the urethelial tract generally.45 Since the
analgesic has been banned in the UK, this is at best, a historical risk. Genetic
susceptibility is associated with bladder cancer aetiology. It is not known whether this
genetic susceptibility varies geographically and so whether it contributes to the overall
pattern of distribution. The geographical distribution of bladder cancer in the UK is
unlikely to be influenced by any of these factors.
KIDNEY CANCER
About 85 per cent of kidney cancers are renal cell carcinomas, with most of the
remaining cases being transitional cell carcinomas of the renal pelvis and ureter. Renal
cell carcinomas have a tendency to spread to other parts of the body via the blood
stream rather than the lymph nodes, giving rise to metastases, particularly in the lungs.
For cancer of the renal pelvis and ureter, studies have found that cigarette smoking is a
major risk factor,46-48 although for renal cell carcinoma, the association with smoking is
weaker.48-52 The use of phenacetin-containing analgesics is a major risk factor for cancer
17
of the renal pelvis and ureter,53 but there are no current UK Marketing Authorisations
(product licenses) for any products containing phenacetin as an active substance.
There is evidence of increased risk of renal cell carcinoma with excess body weight 51,5456
and since the prevalence of obesity is increasing in the UK population, it may have
contributed to the increasing incidence.57 In addition, medications related to the
treatment of hypertension or the severity of hypertension itself are also possible risk
factors.58
For patients who undergo renal dialysis, there is increased incidence of acquired cystic
disease of the kidney, which predisposes to kidney cancer, particularly in males.59 While
inherited factors such as von Hippel-Lindau Syndrome60 are very rare, these patients
develop multiple types of cancer and are thus at greater risk of developing kidney
cancer.
Although the main treatment is surgery, kidney cancer responds to biological treatments,
the main ones being interleukin-2 and interferon. Kidney cancer is, however, not very
responsive to chemotherapy or radiotherapy.
18
HEALTH STATISTICS WALES
The Welsh Health Survey relies on a self-completed questionnaire. The results,
therefore, reflect people’s own understanding of their health rather than a clinical
assessment of their medical condition, and their own interpretation of the health services
they have used.
The survey results are weighted to take account of unequal selection probabilities, and
for differential non-response. The following data is taken from Health Statistics Wales
(2006, National Assembly for Wales).
Table 5 shows health related lifestyle age standardised statistics for adults by Unitary
Authority in Wales, 2003-2005.
Table 5: Health related lifestyle (adults) by Unitary Authority, 2003-2005 (a).
Smoking
Alcohol
consumption
(b)
Binge
drinking
(c)
Unitary Authority
Isle of Anglesey
Gwynedd
Conwy
Denbighshire
Flintshire
Wrexham
28
31
28
26
26
26
37
39
35
35
37
39
16
17
17
17
17
19
44
42
43
42
39
40
33
35
31
32
30
25
52
52
51
50
53
57
Powys
Ceredigion
Pembrokeshire
Carmarthenshire
Swansea
Neath Port Talbot
24
26
26
28
26
29
38
33
38
37
40
45
19
14
16
16
19
20
45
46
43
43
38
40
36
37
33
30
26
26
51
49
55
54
53
56
Bridgend
The Vale of Glamorgan
Cardiff
Rhondda; Cynon; Taff
Merthyr Tydfil
Caerphilly
Blaenau Gwent
Torfaen
Monmouthshire
Newport
29
25
27
28
27
28
31
29
22
26
44
40
39
45
48
42
47
41
35
38
22
19
21
24
22
21
23
20
20
20
38
43
41
35
38
36
35
36
43
38
29
28
27
25
29
25
27
27
32
29
57
53
53
60
58
56
59
56
49
54
Wales
Source: Welsh Health Survey
27
40
19
40
29
54
Consumption
Physical Overweight
of fruit and
activity (e)
or obese
vegetables (d)
(a) Observed percentages are shown here, for age-standardised percentages see the Welsh Health Survey
report. For details of measures (eg units, portions) used please see note at beginning of chapter.
(b) Usual alcohol consumption above daily guidelines.
(c) Alcohol consumption on heaviest drinking day in previous week above 'binge drinking' threshold.
(d) Met guidelines the previous day.
(e) Met guidelines the previous week.
19
Smoking: Those who smoke at least occasionally.
Alcohol consumption: The advice is that men should not drink more than 4 units of alcohol per
day, and women should drink no more than 3 units of alcohol per day. These daily benchmarks
apply whether you drink every day, once or twice a week, or occasionally.
A unit of alcohol is 10ml of pure alcohol.
The list below shows the number of units of alcohol in common drinks:• 1 pint of ordinary strength beer, lager, stout, cider or shandy = 2 units
• 1 pint of strong beer, lager, stout or cider = 3 units
• 1 small glass of wine, sherry or vermouth = 1 unit
• Single spirit measure (whisky, gin, vodka etc) = 1 unit
• 1 alcopop = 1.5 units
Binge drinking: twice daily guidelines (ie more than 8 units for men, more than 6 units for
women).
Consumption of fruit and vegetables: Guidelines are that 5 or more portions should be eaten
per day.
Physical activity: Undertaking physical activity according to the guidelines of at least 30 minutes
of moderate or vigorous physical activity, at least 5 days a week. The 30 minutes can be built up
in blocks of at least 10 minutes. Examples of each type of activity are:
• light activity – housework or golf;
• moderate activity – heavy gardening or fast walking;
• vigorous activity – running or aerobics.
Overweight or obese: The Body Mass Index (BMI) estimates how healthy our weight is, given
our height. However it does not distinguish between mass due to body fat and mass due to
muscular physique, nor does it take account of the distribution of fat. It is calculated as your
weight in kilograms divided by the square of your height in metres. A person is classed as
overweight or obese if the BMI is 25 or more.
Height and weight of respondents are self-reported, and there is evidence to show that some
people tend to under-report weight and/or over-report height, resulting in an under-estimation of
the prevalence of overweight and obesity (Roberts, 199561).
The Cancer Atlas of the UK and Ireland states that cigarette smoking is a major risk
factor for bladder cancer and kidney cancer. The Welsh Health Survey results show
areas in North Wales and South East Wales having the highest smoking rates, the
highest being in Gwynedd and Blaenau Gwent. North Wales is the area with highest
incidence rates of bladder cancer for both males and females. North Wales and Mid and
West Wales have the highest rates for male kidney cancer and South East Wales have
the highest rates of female kidney cancer.
REFERENCES
20
1. Parkin DM, Whelan SL, Ferlay J, Teppo L et al. Cancer Incidence in FiveContinents Vol. VIII.
IARC Scientific Publications No. 155. Lyon: International Agency for Research on Cancer, 2000.
2. Key TJ, Allen N, Appleby P, Overvad K et al. Fruits and vegetables and prostate cancer: no
association among 1104 cases in a prospective study of 130544 men in the European
Prospective Investigation into Cancer and Nutrition (EPIC). International Journal of Cancer 2004;
109: 119-124.
3. Okasha M, McCarron P, McEwen J, Smith GD. Body mass index in young adulthood and
cancer mortality: a retrospective cohort study. Journal of Epidemiology and Community Health
2002; 56: 780-784.
4. Leitzmann MF, Platz EA, Stampfer MJ, Willett WC et al. Ejaculation frequency and subsequent
risk of prostate cancer. Journal of the American Medical Association 2004; 291: 1578-1586.
5. Harding S, Rosato M. Cancer incidence among first generation Scottish, Irish, West Indian and
South Asian migrants living in England and Wales. Ethnicity and Health 1999; 4: 83-92.
6. Breslow N, Chan CW, Dhom G, Drury RA et al. Latent carcinoma of prostate at autopsy in
seven areas. The International Agency for Research on Cancer, Lyon, France. International
Journal of Cancer 1977; 20: 680-688.
7. Power DA, Brown RS, Brock CS, Payne HA et al. Trends in testicular carcinoma in England
and Wales, 1971-99. BJU International 2001; 87: 361-365.
8. Cartwright RA, Elwood PC, Birch J, Tyrell C et al. Aetiology of testicular cancer: association
with congenital abnormalities, age at puberty, infertility, and exercise. British Medical Journal
1994; 308: 1393-1399.
9. Swerdlow AJ, De Stavola BL, Swanwick MA, Mangtani P et al. Risk factors for testicular
cancer: a case-control study in twins. British Journal of Cancer 1999; 80: 1098-1102.
10. Swerdlow AJ, Stavola B, Swanwick M, Mavconochie N. Risks of breast and testicular cancers
in young adult twins in England and Wales: evidence on prenatal and genetic aetiology. Lancet
1997; 350: 1723- 1728.
11. Moller H, Evans H. Epidemiology of gonadal germ cell cancer in males and females. Acta
Pathologica, Microbiologica et Immunologica Scandinavica Supplement 2003; 111: 43-46.
12. Skakkebaek NE, Berthelsen JG, Giwercman A, Muller J. Carcinoma-insitu of the testis:
possible origin from gonocytes and precursor of all types of germ cell tumours except
spermatocytoma. International Journal of Andrology 1987; 10: 19-28.
13. Moller H, Skakkebaek NE. Testicular cancer and cryptorchidism in relation to prenatal factors:
case-control studies in Denmark. Cancer Causes and Control 1997; 8: 904-912.
14. Richiardi L, Akre O, Bellocco R, Ekbom A. Perinatal determinants of germ-cell testicular
cancer in relation to histological subtypes. British Journal of Cancer 2002; 87: 545-550.
15. Jacobsen R, Bostofte E, Engholm G, Hansen J et al. Risk of testicular cancer in men with
abnormal semen characteristics: cohort study. British Medical Journal 2000; 321: 789-792.
16. Schottenfeld D. Testicular cancer. In: Schottenfeld D, Fraumeni JF, Jr. (eds) Cancer
Epidemiology and Prevention. New York: Oxford University Press, 0 AD.
17. Forman D, Oliver RT, Brett AR, Marsh SG et al. Familial testicular cancer: a report of the UK
family register, estimation of risk and an HLA class 1 sib-pair analysis. British Journal of Cancer
1992; 65: 255- 262.
18. Parkin DM, Whelan SL, Ferlay J, Teppo L et al. Cancer Incidence in Five Continents Vol. VIII.
IARC Scientific Publications No. 155. Lyon: International Agency for Research on Cancer, 2000.
19. Quinn MJ, Babb PJ, Brock A, Kirby L et al. Cancer Trends in England and Wales 1950-1999.
Studies on Medical and Population Subjects No. 66. London: The Stationery Office, 2001.
20. Wynder E, Stellman S. Environmental factors in the causation of bladder cancer. In: Connolly
J (ed) Carcinoma of the Bladder. New York: Raven Press, 1981.
21. Ross RK, Paganini-Hill A, Hendersen BE. Epidemiology of bladder cancer. In: Skinner DG,
Lieskovsky G (eds) Diagnosis and Management of Genitourinary Cancer. Philadelphia: W.B.
Saunders Co., 1988.
22. Doll R, Peto R. Mortality in relation to smoking: 20 years’ observations on male British
doctors. British Medical Journal 1976: 1525-1536.
23. Hartge P, Silverman D, Hoover R, Schairer C et al. Changing cigarette habits and bladder
cancer risk: a case-control study. Journal of the National Cancer Institute 1987; 78: 1119-1125.
21
24. Hartge P, Silverman DT, Schairer C, Hoover RN. Smoking and bladder cancer risk in blacks
and whites in the United States. Cancer Causes and Control 1993; 4: 391-394.
25. Bartsch H, Caporaso N, Coda M, Kadlubar F et al. Carcinogen hemoglobin adducts, urinary
mutagenicity, and metabolic phenotype in active and passive cigarette smokers. Journal of the
National Cancer Institute 1990; 82: 1826-1831.
26. Bryant MS, Vineis P, Skipper PL, Tannenbaum SR. Hemoglobin adducts of aromatic amines:
associations with smoking status and type of tobacco. Proceedings of the National Academy of
Sciences of the USA 1988; 85: 9788-9791.
27. Patrianakos C, Hoffmann D. Chemical studies of tobacco smoke. LXIV. On the analysis of
aromatic amines in cigarette smoke. Journal of Analytical Chemistry 1979; 3: 150-154.
28. Vineis P, Esteve J, Hartge P, Hoover R et al. Effects of timing and type of tobacco in
cigarette-induced bladder cancer. Cancer Research 1988; 48: 3849-3852.
29. Case RA, Hosker ME, McDonald DB, Pearson JT. Tumours of the urinary bladder in workmen
engaged in the manufacture and use of certain dyestuff intermediates in the British chemical
industry. I. The role of aniline, benzidine, alpha-naphthylamine, and betanaphthylamine. British
Journal of Industrial Medicine 1954; 11: 75- 104.
30. Case RA, Hosker ME. Tumour of the urinary bladder as an occupational disease in the rubber
industry in England and Wales. British Journal of Preventative and Social Medicine 1954; 8: 3950.
31. Kogevinas M, Sala M, Boffetta P, Kazerouni N et al. Cancer risk in the rubber industry: a
review of the recent epidemiological evidence. Occupational and Environmental Medicine 1998;
55: 1-12.
32. Vineis P, Magnani C. Occupation and bladder cancer in males: a casecontrol study.
International Journal of Cancer 1985; 35: 599-606.
33. Bethwaite PB, Pearce N, Fraser J. Cancer risks in painters: study based on the New Zealand
Cancer Registry. British Journal of Industrial Medicine 1990; 47: 742-746.
34. Steenland K, Palu S. Cohort mortality study of 57,000 painters and other union members: a
15 year update. Occupational and Environmental Medicine 1999; 56: 315-321.
35. Hoar SK, Hoover R. Truck driving and bladder cancer mortality in rural New England. Journal
of the National Cancer Institute 1985; 74: 771- 774.
36. Theriault G, De Guire L, Cordier S. Reducing aluminum: an occupation possibly associated
with bladder cancer. Canadian Medical Association Journal 1981; 124: 419-22, 425.
37. Coggon D, Pannett B, Acheson ED. Use of job-exposure matrix in an occupational analysis of
Lung and Bladder cancers, on the basis of death certificates. Journal of the National Cancer
Institute 1984; 72: 61-65.
38. Dolin PJ. A descriptive study of occupation and bladder cancer in England and Wales. British
Journal of Cancer 1992; 65: 476-478.
39. Baxter PJ, McDowell ME. Occupation and cancer in London: an investigation into nasal and
bladder cancer using the Cancer Atlas. British Journal of Industrial Medicine 1986; 43: 44-49.
40. Travis LB, Curtis RE, Glimelius B, Holowaty EJ et al. Bladder and kidney cancer following
cyclophosphamide therapy for non-Hodgkin’s lymphoma. Journal of the National Cancer Institute
1995; 87: 524- 530.
41. Boice JD, Jr., Engholm G, Kleinerman RA, Blettner M et al. Radiation dose and second
cancer risk in patients treated for cancer of the cervix. Radiation Research 1988; 116: 3-55.
42. Chiang HS, Guo HR, Hong CL, Lin SM et al. The incidence of bladder cancer in the black foot
disease endemic area in Taiwan. British Journal of Urology 1993; 71: 274-278.
43. Cuzick J, Sasieni P, Evans S. Ingested arsenic, keratoses, and bladder cancer. American
Journal of Epidemiology 1992; 136: 417-421.
44. Wilkins JR, III, Comstock GW. Source of drinking water at home and site-specific cancer
incidence in Washington County, Maryland. American Journal of Epidemiology 1981; 114: 178190.
45. Piper JM, Tonascia J, Matanoski GM. Heavy phenacetin use and bladder cancer in women
aged 20 to 49 years. New England Journal of Medicine 1985; 313: 292-295.
46. McLaughlin JK, Silverman DT, Hsing AW, Ross RK et al. Cigarette smoking and cancers of
the renal pelvis and ureter. Cancer Research 1992; 52: 254–257.
22
47. Jensen OM, Knudsen JB, McLaughlin JK, Sorensen BL. The Copenhagen casecontrol study
of renal pelvis and ureter cancer: role of smoking and occupational exposures. International
Journal of Cancer 1988; 41: 557–561.
48. McCredie M, Stewart JH. Risk factors for kidney cancer in New South Wales. I. Cigarette
smoking. European Journal of Cancer 1992; 28A: 2050–2054.
49. McLaughlin JK, Mandel JS, Blot WJ, Schuman LM et al. A population-based case-control
study of renal cell carcinoma. Journal of the National Cancer Institute 1984; 72: 275–284.
50. La Vecchia C, Negri E, D’Avanzo B, Franceschi S. Smoking and renal cell carcinoma. Cancer
Research 1990; 50: 5231–5233.
51. Kreiger N, Marrett LD, Dodds L, Hilditch S et al. Risk factors for renal cell carcinoma: results
of a population-based case-control study. Cancer Causes and Control 1993; 4: 101–110.
52. Mellemgaard A, Engholm G, McLaughlin JK, Olsen JH. Risk factors for renal cell carcinoma in
Denmark. I. Role of socioeconomic status, tobacco use, beverages, and family history. Cancer
Causes and Control 1994; 5: 105–113.
53. McCredie M, Stewart JH, Day NE. Different roles for phenacetin and paracetamol in cancer of
the kidney and renal pelvis. International Journal of Cancer 1993; 53: 245–249.
54. Bergstrom A, Pisani P, Tenet V, Wolk A et al. Overweight as an avoidable cause of cancer in
Europe. International Journal of Cancer 2001; 91: 421–430.
55. Mellemgaard A, Engholm G, McLaughlin JK, Olsen JH. Risk factors for renalcell carcinoma in
Denmark. III. Role of weight, physical activity and reproductive factors. International Journal of
Cancer 1994; 56: 66–71.
56. McCredie M, Stewart JH. Risk factors for kidney cancer in New South Wales, Australia. II.
Urologic disease, hypertension, obesity, and hormonal factors. Cancer Causes and Control 1992;
3: 323–331.
57. Seidell JC, Flegal KM. Assessing obesity: classification and epidemiology. British Medical
Bulletin 1997; 53: 238–252.
58. Heath CW, Jr., Lally CA, Calle EE, McLaughlin JK et al. Hypertension, diuretics, and
antihypertensive medications as possible risk factors for renal cell cancer. American Journal of
Epidemiology 1997; 145: 607–613.
59. Ishikawa I. Development of adenocarcinoma and acquired cystic disease of the kidney in
hemodialysis patients. Princess Takamatsu Symposium 1987; 18: 77–86.
60. Latif F, Tory K, Gnarra J, Yao M et al. Identification of the von Hippel-Lindau disease tumor
suppressor gene. Science 1993; 260: 1317–1320.
61. Roberts RJ (1995) Can self-reported data accurately describe the prevalence of overweight?
Journal of Public Health 109(4); 275-284
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