&EPA
United States
Environmental Protection
Agency
Environmental Monitoring
and Support Laboratory
P. 0 Box 15027
Las Vegas NV 89114
EPA-600/1-79-022
June 1979
Research and Development
Preliminary Analysis
of Cancer Rates in
Primary Organic
Chemical-Producing
Counties
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RESEARCH REPORTING SERIES
Research reports of the Office of Research and Development, U.S. Environmental
Protection Agency, have been grouped into nine series. These nine broad cate-
gories were established to facilitate further development and application of en-
vironmental technology. Elimination of traditional grouping was consciously plan-
ned to foster technology transfer and a maximum interface in related fields. The
nine series are:
1. Environmental Health Effects Research
2. Environmental Protection Technology
3. Ecological Research
4. Environmental Monitoring
5. Socioeconomic Environmental Studies
6. Scientific and Technical Assessment Reports (STAR)
7. Interagency Energy-Environmental Research and Development
8. "Special" Reports
9. Miscellaneous Reports
This report has been assigned to the ENVIRONMENTAL HEALTH EFFECTS RE-
SEARCH series. This series describes projects and studies relating to the toler-
ances of man for unhealthful substances or conditions. This work is generally
assessed from a medical viewpoint, including physiological or psychological
studies. In addition to toxicology and other medical specialties, study areas in-
clude biomedical instrumentation and health research techniques utilizing ani-
mals—but always with intended application to human health measures.
This document is available to the public through the National Technical Informa-
tion Service, Springfield, Virginia 22161
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EPA-600/1-79-022
June 1979
PRELIMINARY ANALYSIS OF CANCER RATES IN ORGANIC
CHEMICAL-PRODUCING COUNTIES
By
Amy J. Cross and G. Bruce Wiersma
Monitoring Systems Research and Development Division
Environmental Monitoring and Support Laboratory
P. 0. Box 15027
Las Vegas, Nevada 89114
ENVIRONMENTAL MONITORING AND SUPPORT LABORATORY
OFFICE OF RESEARCH AND DEVELOPMENT
U.S. ENVIRONMENTAL PROTECTION AGENCY
LAS VEGAS, NEVADA 89114
-------
DISCLAIMER
This report has been reviewed by the Environmental Monitoring and
Support Laboratory-Las Vegas, U.S. Environmental Protection Agency, and
approved for publication. Mention of trade names or commercial products
does not constitute endorsement or recommendation for use.
ii
-------
FOREWORD
Protection of the environment requires effective regulatory actions
that are based on sound technical and scientific information. This infor-
mation must include the quantitative description and linking of pollutant
sources, transport mechanisms, interactions, and resulting effects on man
and his environment. Because of the complexities involved, assessment of
specific pollutants in the environment requires a total systems approach
that transcends the media of air, water, and land. The Environmental
Monitoring and Support Laboratory-Las Vegas contributes to the formation
and enhancement of a sound monitoring data base for exposure assessment
through programs designed to:
develop and optimize systems and strategies for moni-
toring pollutants and their impact.on the environment
• demonstrate new monitoring systems and technologies by
applying them to fulfill special monitoring needs of
the Agency's operating programs
This study is designed to determine whether there is an association
between cancer mortality and the industrial production of environmental
carcinogens. Mortality rates in counties containing organic chemical
production facilities are compared to rates in control counties. The
study aids in the development of statistical techniques for determining
the contribution of environmental contaminants to the rise in cancer
rates. Research of this type assists in the identification of compounds
that need to be regulated. For further information, contact the Monitor-
ing Systems Research and Development Division of the Laboratory.
GeorgjTB/ Morgan */
Director
Environmental Monitoring and Support Laboratory
Las Vegas
iii
-------
SUMMARY
This study is designed to determine whether there is an association
between cancer mortality and the production of environmental carcinogens.
Mortality rates of counties containing organic chemical production facilities
are compared to rates of control counties. Twelve different cancer sites in
lung, stomach, etc., and eight organic carcinogens were considered. Although
a rigorous statistical analysis, was not conducted, for most cancer sites mor-
tality rates were found to be higher in counties of organic carcinogen pro-
duction than in control counties. The study aids in the development of sta-
tistical techniques for .determining the contribution of environmental contam-
inants to the rise in cancer rates. Research of this type assists in the
identification of compounds that need to be regulated.
iv
-------
INTRODUCTION
The literature indicates an increase in cancer mortalities in chemical-
producing counties (CPCs). Mason's report (1975) shows that a high rate of
multiple myeloma and liver cancer occurs in vinyl chloride workers. A study
by Hoover and Fraumeni (1975) relates a significant risk in male lung cancer
with CPCs. Hoover et al. (1975) correlates cancers of the large intestine,
rectum, esophagus, and bladder as a complex of urbanization.
An investigation (Kwalick et al., 1976) of New Jersey cancer mortalities
cites this state as the most cancer-prone. The author suggests population
density, industrialization, and a high concentration of organic chemical
producers in the state as possible etiologic factors.
Figure 1 shows the location of primary organic chemical producers in
the United States. When compared to Figure 2, which was taken from data in
the cancer atlas (Mason et al., 1975), a relationship is suggested between
organic chemical production and higher than average lung cancer mortality
rates. Comparison of Figure 1 to other maps extracted from the cancer atlas
for cancers of the large intestine, rectum, liver, and female breast illu-
strates similar relationships. Comparison of a population density map to
the map for lung cancer (Figure 2) also shows a correlation.
Several problems complicate a statistical analysis of cancer incidence.
Since no record of cancer incidence exists for any number of years, mortality
data are used as an indication-of incidence (Hoover and Fraumeni, 1975;
Hoover et al., 1975; Mason, 1975). A certain amount of error is involved
in the assumption that mortalities are indicative of incidence, most obvious
of which is the fact that medical advances are lowering the mortality rates
while the incidence rates rise (Levin et al., 1974). Mortality rates may
not reflect the county of exposure since each neoplasm is recorded by county
of death, not by county of residence and/or exposure. Differences in medical
diagnosis of primary and secondary causes of death also inject error into the
data.
Other problems involved in this type of analysis include variability in
industrial processes, possible synergistic effects of chemicals, bias toward
industries which dominate the employment of counties, and bias toward indus-
tries with variability in exposure. Limitations of a statistical study of
site-specific cancer mortalities in relation to any other variable include
non-industrial correlates: smoking habits, dietary differences, hormonal
factors, cancer induction-related diseases, urbanization, meteorology, the
latency period of cancers, sex, and age (Hoover and Fraumeni, 1975> Hoover
et al., 1975; Mason, 1975; and Levin et al., 1974).
-------
1. Phenol
2. Benzene
3. Tetraethyl lead
4. Chloroform
5. Ethanol
6. Vinyl chloride
7. Carbon tetrachloride
8. Formaldehyde
Figure 1. Locations of Chemical Producing Counties
-------
Figure 2.
Counties of significantly high trachea, bronchus, and lung cancer
mortalities 1950-1969.
-------
In spite of the cautions involved in relating cancer incidence with
cancer mortality data, such relationship still provides the most accessible
and systematic means of studying the hazards associated with potential car-
cinogens in the environment. Basic statistics are used descriptively in this
study, not in hypothesis testing.
CONCLUSIONS
Comparisons of the mean cancer mortality rates of chemical-producing
counties, non-chemical-producing counties (non-CPCs), and the nation support
reports of increased cancer rates in CPCs. In 284 comparions, 205 CPC mean
cancer rates were higher than the non-CPC rates. ,In the same number of com-
parisons to U.S. mean cancer mortalities, 113 CPC rates were higher (Table 1).
Specifically, the study supports statistical investigations in which
rates of cancers of the lung, large intestine, rectum, esophagus, breast,
stomach, corpus uteri, cervix uteri, leukemia-aleukemia, total cancer, and
multiple myeloma (vinyl chloride CPCs observed only) were found-to be higher
in CPCs than in non-CPCs.
The CPCs with most excessive and numerous mean cancer rate differences
from the non-CPCs and the nation were those producers of phenol, tetraethyl
lead, ethanol, benzene, chloroform, formaldehyde, and carbon tetrachloride.
Population density was shown to play a significant role in the results
of this study. The CPCs were found to have a significantly higher population
density than the non-CPCs. This also supports a report in which urbanization
is correlated to a complex of cancers of the bladder, large intestine, rectum,
and esophagus.
RECOMMENDATIONS
Both the literature and this study indicate that cancer mortality rates
for the CPCs of phenol, benzene, vinyl chloride, chloroform, tetraethyl lead,
ethanol, possibly formaldehyde, and possibly carbon tetrachloride should be
included in the data of a more conclusive statistical analysis. However,
the widespread use of ethanol in a non--indus trial manner may impose the
requirement for different or additional statistical treatment. Studies sug-
gest also that the cancer sites to be studied in relation to these CPCs be
the large intestine, rectum, liver, lung, female breast, esophagus, stomach,
leukemia-aleukemia, corpus uteri, cervix uteri, bladder, total cancer, and
possibly multiple myeloma."
This analysis should include a ^control of non-industrial correlates of
carcinogenesis (System Sciences, Inc., 1975). The data could then be analyzed
by factor analysis and three-way analysis of variance. Factor analysis would
serve to eliminate the high correlation between variables that cause the.(
regression computations to numerically break down. Instead of the gairexL
T-test, three-way analysis of variance would be used to separate the causes
of significance because it can handle more^than two groups.. A test for
-------
TABLE 1. MEAN CANCER RATES OF U.S., NON-CPCs, AND CPCs
•
-8
*j a
5,3
8
(U i-l
60 *J
u ta
AS
&
JJ
I
So
CO
X
s ,
w
10
BO
!•
s
2
«
.e
o
4J
V)
"b £
°" s
t i
f> ?
•b!
fV- ?
•b s
"*&
•b ;
0* g
if S
- >s
°*
•b ;
&
» •
•
NATION
174.04
184.28
130.10
139.18
16.54
12.07
. 16.25
'••- !12.69
3 '. 7.65
5.68
4.82
4.46
4.10
9.44
_« 1.03 >
2'.1^*C
3 7. $$43'
36.67^"
6.297' '
•6.27'
25.51
22.10.
15.22
24.03
7.70
in. fid
Chloroform
NON-CPC
160.433
106.98
116.26
135.16
13.1
7.65
15.06
21.6
4.467
1.400
3.600
.850
2'. 620
;5.600
[ .520
.380
37.900
24.750
20.233'
4.4
17*-9
, 18-
13.960^
18.475
6.96
5.925
CPC
*173.5*5*
138.940
126.38
126.6
14.4
* **
16.050
13.52
8.55
* 5.217
* 4.125
3.420
3.875
3.460
9.050
* **
1.080
* 2.855*
*42.65**
*33.500
*23.250*
* ..7
*
. 21.4
- 14.94
~'i'3.220
*30.82?*
6.66
8,475
Benzene
NON-CPC
158.326
163.889
113.993
114.936
13.446
16.489
12.026
10.254
4.870
7.036
4.464
2.793
3.107
7.961
.843
1.446
36.544
37.982
5.818
7.000
18.500
15.779
13.485
23.868
7.921
9.361
CPC
1.78. 3*ti
* **
191.077
122.425
1.36.007
14.711
10.441
14.607
* **
12.934
* 6.322
5.7*:!
4.159
3.941
3.557
7.811
*
.977
*
1.757
* **
45.715
*45.801
* **
6.629
4r itir
7.573
22.400
20.071
*14.038
*25.5*!
7.250
10.279
Ethanol
NON-CPC
157.583
141.160
113.660
120.250
12.767
12.325
14.08
10.550
5.700
2.675
2.680
1.825
3.260
6.000
.816
1.600
35.850
34.850
6.26
5.600
19 . 660
17.500
10.820
21.225
6.54
12.150
CPC
* **
183.317
164.88
"5 **
131.580
* **
143.300
16.183
* **
12.45
* **
16.32
* **
13.125
* 7.017
* 6.1*2*5
4.260
* **
4.925
3.800
9.400
.820
1.700
* *#
43.400
*43.2«
* **
7.660
7.050
*
23.380
*24.5*.*>
*13.160
25.800
*
6.68
10.075
Tetracthyl Lead
NON-CPC
171.300
157.233
119.983
129.467
13.4
9.767
14.133
9.900
5.35
3.95
3.717
5.433
3.850
6.750
2.017
2.017
40.22
34.417
6.933
8.117
20.233
20.55
16.733
20.300
8.300
11.767
CPC
* **
183.233
* **
194.217
127.733
136.583
14.35
11.050
15.133
11.083
5.25
4.167
3.800
**
4.467
* *dr
4.317
7.550
1.183
» **
2.500
w ww
46.32
* **
41.67
* **
7.383
7.233
••*
23.250
21.233
12.850
* **
25.883
6.567
* **
11.800
Phenol
NON-CPC
165.818
164.036
121.155
101.836
14.218
7.027
14.464
10.927
6.518
5.673
4.109
2.064
3.836
6.427
.755
.964
34.918
27.045
6.336
4.527
20.755
14.427
15.582
39.364
7.300
6.645
CPC
* **
181.327
* **
192.500
129.050
130.682
15.482
* **
14.418
15.682
it irtt
18.282
6.455
4.045
4.018
3.273
* **
4.109
7.655
.964
1.209
* **
42.905
*49.70*9*
* • **'
6.650
6.336
— w
23.614
16.464
4 AJr
15.741
28.136
TF
7.332
9 . 500
(continued)
-------
TABLE 1. MEAN CANCER RATES OF U.S., NON-CPCs, AND CPCs
!
O AJ
*b g
0* B
n
g
3-1
UtH
rH 41
NATION
5.160
6.910
5.340
4.590
17.840
27.390
*b I
O- *
Chloroform
NON-CPC
6.083
5.280
6.7.30
0.760
16.180
17.033
NATION
1.760
2.700
1.240
1.830
CPC
5.033
6.560
**
5.500
3.280
17.033
21.960
Benzene
NON-CPC
5.282
8.379
5.036
3.286
16.454
27.421
Vinyl Chloride
NON-CPC
1.344
0.938
1.922
0.725
CPC
*2.056**
*2.400
1.378**
*1.663
CPC
5.086
6.720
4.659
* **
4.793
17.130
23.920
M
s
0) Q)
O *J
U (0
Pi W
Ethanol
NON-CPC
5.867
7.520
4.560
7.040
18.550
22.640
\> I
*
g
* *
° g
•CPC
s.ieV
6.180
* 4.920
3.980
17.95*)*
22.240
NATION
5.160
6.910
5.340
4.590
17.840
27.390
Tetraethyl Lead
NON-CPC
7.083
6.983
4.800
3.800
15.933
22.500
CPC
5.367*
* 7.28V
4.400
* 5.48?*
* 18.40*0*
* **
28.850
Formaldehyde
NON-CPC
5.189
7.191
4.989
4.266
16.649
23./I&1
CPC
* 5.423**
* 7.978**
4.918
* 4.686**
* 17. 893**
22.586
Phenol
NON-CPC
5.291
4.655
5.400
2.482
17.036
24.718
CPC
5.159
* 6.63*
4.686
* 5.04?*
15.159
24.127
Carbon
Tetrachloride
NON-CPC
5.691
3.750
5.682
4.470
17.045
20.340
CPC
Ant
5.336
* 7.74*3*
5.118
3.490
16.773
* 22. 860
(continued)
-------
TABLE 1. MEAN CANCER RATES OF U.S., NON-CPCs, AND CPCs
Cervix
Uteri
Corpus
Uteri
Leukemia-
Aleukemia
0* f
o I
r>-
BB
o *
3
NATION
8.B1
5.77
5.74
3.88
6.13
11.3
7.79
18.92
Chloroform
NON-CPC
8.880
3.250
5.240
2.750
6.240
5.075
9.720
12.125
CPC
* **
9.220
* **
6.700
5.560
2.025
**
6.180
7.975
* 10. 34*0*
13.250
Benzene
NON-CPC
8.686
3.900
5.279
2.650
6.107
10.886
7.446
21.032
CPC
8.727
* 5.188
*5.611
*4.59**
5.513
10.470
* 7.85*6*
17.173
Ethanol
NON-CPC
10.200
9.050
5.240
4.600
5.700
10.925
7.640
11.650
CPC
10.020
6.6**
*6.4**
4.10*6*
* 6.8**
10.225
* 7.8*0*
17.375
Tetraethyl Lead
NON-CPC
8.250
4.317
5.033
6.100
6.400
8.150
8.683
14.517
CPC
* **
9.600
* 5.400
JL JLJL
6.100
**
4.317
5.617
*11.530
**
7.833
14.850
Phenol
NON-CPC
9.J73
4.727
5.573
3.682
6.745
6.127
7.618
13.018
CPC
8.532
4.900
* **
6.114
* **
3.973
6.282
*11.064
* **
8.545
13.418
(continued)
-------
4-)
c
o
u
0)
o
dn
O
0)
u
Y
S3
rH M
g)
3,
0)
D.
O
CO -
W
to
60
1
CO
CO
0)
M
pa
u
4J
m
i a)
ill
J 13.25
CPC
* 169.72
* 174.46
* 123.35
129.47
* 14.29
* 11.75
* 14.46
12.16
* 6.36
* 6.»
* 3.95
4.16
* 4.2?
* 8.67
* 1 M
* 1.70
* 39.38
* 37.20
5.70
5.28
* 23.38
19.58
* 13.49
* 22.11
* 6.97
* 9.71
5.78
* 5 &&
* 9.00
* 4.fet
8.5?
* 17.83
* 5.85
* 10.03
Carbon
Tetrachloride
NON-CPC
158.47
139.50
113.99
117.72
11.34
11.59
12.72
, 6.87
3.91
2.35
3.25
2.40
2.70
6.55
1.78
0.42
38.70
31.41
6.17
7.43
18.11
27.92
14.50
16.64
7.37
9.71
5.75
3.48
7.36
2.58
9.93
17.46
5.21
• 7.75
CPC
* 177. Ti
* 173.54
* 122.44
* 141?9*8
* 14.31
11.36
* 14.76
* 8.44
* 5.44
* 4.10
* 3.52
* 3.24
* 3.67
* 6.63
iffe
* 2*41
* 45.58
* 38^§5
* 6*?8
6*9*3
* 21.78
16.78
14.45
* 25T?1
6.86
.9.61
* 5.76
* e!?2
* 8T?2
* 3.28
9?*3
16*^2
* 5.70
* 10.94
•u
(U
I
4J
§
U
I
-------
normality of raw data would be requisite to all testing.
The findings from these analyses would be utilized in narrowing the
field of choices of organic chemicals and their related cancer sites for
pathways studies.
METHODS AND MATERIALS
The purposes of this study are to: 1) assist in the selection of candi-
date organic chemicals which are carcinogens or suspected carcinogens suitable
for pathways studies; 2) determine if a relationship exists between cancer
incidence and the organic chemical industry; and 3) aid in development of a
statistical method of relating disease incidence to industry.
The 1977 Registry of Toxic Effects of Chemical Substances (Fairchild
et al., 1977) was used to identify potentially carcinogenic and carcinogenic
chemicals in the U.S. Information on 400 organic industrial chemicals and
their 610 production locations was obtained from the Organic Chemical Pro-
ducers' Data Base Program (Garner and Dzierlenga, 1976). This program in-
cludes data, when available, for each chemical on toxicity, production volumes,
costs, emission factors, cross-indexed chemical tree, and Wiswesser Line Nota-
tion. Each production plant is classified according to original feedstock
source, product slate, and whether it is refinery associated. Plant-specific
information on each chemical includes production capacities, and production
routes (Wilkins, 1976).
The carcinogenic chemicals selected were those having more than three
production locations and whose production capacity was available. The list
of chemicals includes benzene, phenol, carbon tetrachloride, formaldehyde,
chloroform, tetraethyl lead, ethanol, and vinyl chloride. The CPCs selected
contained producers of one or more of the selected chemicals.
Following a review of the literature, cancer sites chosen for representa-
tive mortality rates were: lung, rectum, stomach, prostate, large intestine,
liver, female breast, esophagus, corpus uteri, cervix uteri, leukemia-aleukemia,
aleukemia, total cancer, and multiple myeloma (for vinyl chloride CPCs only).
Age-adjusted mortality rates/100,000 individual's are available for the years
1950-1969 by sex and race for each CPC (Mason et al., 1975). The analysis
includes counties not classified as a CPC of any of the listed chemicals,
increasing the data spread and minimizing bias. A random number table facili-
tated the selection of a county adjacent to or near such CPC, designated a
non-CPC. Any CPC which does not contain a nonwhite population was excluded
from 'calculations of the nonwhite cancer rates. The nearness of CPCs to non-
CPCS lessens variation due to differences in lifestyles, meteorological
variation$ and urbanization. This may allow for exposure of the non-CPCs
to the chemical of the analysis.
A paired T-test of cancer rates by organic chemical and linear regression
analysis of such numerous production volumes and cancer rates are statisti-
cally invalid, by simultaneous inference. A large number of tests performed
makes possible simultaneous-statistical inferences (R. R. Rinnison, personal
-------
communication). Mortality means were calculated of each site-specific cancer
for all CPCs and non-CPCs.
These calculations and national cancer mortality means (Mason and McKay,
1974) were compared in order to determine whether a difference exists between
cancer rates in the CPCs and non-CPCs chosen. The national means were used
in conjunction with non-CPC values as a control.
RESULTS AND DISCUSSION
In 284 comparisons between mean cancer mortalities of CPCs and non-CPCs,
205 CPC means are higher, as shown in Table 1 and illustrated in Figures 3
through 19. Especially higher means occur for nonwhites in tetraethyl lead
CPCs, all males in benzene CPCs, all females in chloroform CPCs, and nonwhite
males in phenol CPCs (Figure 3).
A high rate of a cancer for a sex in both races suggests occupational
exposures to cancer-causing agents encountered in the dissimilar environments
(until recently) of the traditional male/female roles. This possibly explains
the difference between mortality rate means in phenol CPCs for stomach cancer
(Figure 4), tetraethyl lead CPCs for liver cancer (Figure 5), chloroform CPCs
for leukemia-aleukemia (Figure 15), lung cancer in all of the CPCs (Figures
3, 7, and 8), and esophageal cancer in benzene CPCs (Figure 16).
A high rate of cancer for both sexes of only one race suggests exposures
to cancer-causing agents encountered in different ethnic lifestyles because
of dietary differences, alcohol and tobacco intake, differences in blue collar
and white collar occupational exposures, living conditions, etc. Therefore,
influences on non-industrial correlates are suggested by excess mortality
rates of a cancer of either racial group. This is illustrated by stomach
cancer rates in tetraethyl lead and chloroform CPCs (Figure 4), cervix uteri
cancer rates in benzene CPCs (Figure 9), corpus uteri cancer rates in tetra-
ethyl lead CPCs (Figure 5), rectal cancer rates in ethanol CPCs (Figure 6),
rates of cancer of the large intestine in phenol CPCs (Figure 10), total
cancer mortalities in tetraethyl lead, phenol, and ethanol CPCs (Figure 18),
and liver cancer mortalities in phenol, and ethanol CPCs (Figure 18), and
liver cancer mortalities in benzene, chloroform, formaldehyde, and phenol
CPCs (Figures 13 and 19).
Similar comparisons between CPC cancer rates and national mean cancer
rates are given in Table 1. The association of tetraethyl lead production
and mortality is most obvious for nonwhites, noted in esophageal cancer
(Figure 11), stomach cancer (Figure 4), cancer of the large intestine (Figure
10), and lung cancer (Figure 3). , Of the 284 comparisons, 113 mean CPC rates
are higher than the national means (Table 1). Corpus and cervix uteri cancer
rates are higher than the national means in every CPC studied except for
cancer of the corpus uteri in benzene CPCs (Table 1). In addition to tetra-
ethyl lead CPCs (Figures 5 and 17), ethanol CPCs show an excess prostate
cancer and female breast cancer mortality rate for both racial groups over
national means (.Figures 17 and 12). Leukemia-aleukemia rates are higher for
all but nonwhite females in tetraethyl lead CPCs (Figure
10
-------
1
UJ
(L
(2
ZiSO
i
u
AGE-ADJUSTED
S S
10
BENZENE
-------
35
1
i30
oo
—
CD
a a
n
a
| ib
* 10
5
BENZENE
0* 9
W NW W NW
n = 28
m
1
s
3 1
ri •»
I]
PC
*
CK
CK
8
- -i
CK
I
i*i
n
n =
S
±1
CK
28
* 1
i
CK
1*1
CK
CHLOROFORM
o* 9
W NW W NW
n = 6 n = 5'
S
i
g r ~
ri H
ll
CK
ft
CK 55 C
f n = 6 n
|
i
= 5
UH nlon MlaM iMn kin
is i
w
" S. m "
i
i
CK
Cre-CHrjIal PrUuilm Cml> W.WUU
•OICre'to^linlaJPrMBClKCMrf •«-
40
i M
UJ
| 30
1,
2 ;n
f?. 20
i
3 is
10
TETRAETHYL LEAD
o- 9
W NW W NW
n = 6
1
2
- -i
CK
*1
CK
rf
""
CK
E
rin
CK
n = 6
s §
g
•£•
CK
f ^
T
CK
X
CK
PHENOL
0" 9
W NW W NW
n = ll
N —
y T
"i
CK
J.
CK
PI
1
1
1
CK
S
S
CK
§
rt
CK
n =
8
*
CK
11
1
J
~
i
rn
CK
ETHANOL
o- 9
W NW W NW
n=5 n=4
ri
!r
1
a »
1
.-
n
n
CK i
crc CPE
n=5 n=4
S
— 40
rfi?
5 g Tl
T T
T*
CK « JR. tK
cn •OMitii rnmcui c««r
•OK CPC • IvOMICll PrMKUl bMT
Figure 4. Mean age-adjusted stomach cancer mortalities in CPCs and non-CPCs.
12
-------
= 20
BREAST
9
W NW
n = 6
S
tM
ftt
ft
at
1
g
SJ
s
|Ciali W.WMU
101 ere • Mo-ciaicii Pmutmi Cmm iw • «i« wniu
n • feBbw f ObttnnUMi
X 'Slindinl tmr
Mean age-adjusted cancer mortalities in tetraethyl
non-CPCs .
CE
LU
Q.
09
5 10
0
E
1 &
CJ
^
2
S <
2
TETRAETHYL LEAD
o" 9
W NW W NW
n-6
Ills
TO
S c« S «
...
i
113
- Il
T^Trr,
IFI n
s •* s. ^
PHENOL
0*
9
W NW W
n = 11
i i
TT
1
CK
1
cn
g
CK
1
CPC
s
4
CK
n
CO
I
fl
crc
NW
-11
i
crc
CPC-ChmleilPiMiiEloiCiiiuy W-Wtlu • • Inmbn il OMrnlKn
Mil CPC • immulgl ft milil C»»lt l«.l«iWWt« T-ttimfltrr«
5
i
en
ETHANOL
lead CPCs and
0* 9
W NW W
n=5 n=4
1
S_ "
!
CK
~
to
CPC
n
J
CK
•on nlm IKIcitM iMn bin
= 5
cn
NW
n=4
1
ere
*
CK
Figure 6. Mean age-adjusted rectal cancer mortalities in CPCs and non-CPCs.
13
-------
g
oe
UJ
Q_
S
*
w
n=45
3 *
Wf wc
•01 ere
ESOPHAGUS
d* 9
NW W NW
n=44
1
CK
ft
CK
n = 45 n = 44
§i IS
|S|CK||S|«|
LUNGS
o» 9
W NW W NW
n=45 n=44
| s
I
CK
•£|
CK
|
CO
5
*
CK
n=45 n = 44
§ S 2 |
S;(CK| |s|m|
BREAST
9
W NW
n=45 n = 44
1
CK
*
CK
f"
CK
tn
of
CK
CERVIX UTERI
9
W NW
n=45 n = 44
|I
llf
5 « S CK
rrr,r._ ™.. i-^rr— -
£
CO
UJ
t—
J
DJUSTED CANCER MOR
K
tu
S
STOMACH
_j» O
Ct »
W NW W
n =45 n = 44
=
wt
ii
i
CK
[t
5
X
CK
n=45
tt
NW
n =
it
CK
ere . amen nmdn OMT
44
4
CK
LEUKEMIA-ALEUKEMIA
O*
W NW
n = 45 n = 44
3 5 I 3
|CK|EK| I3clt'cl
W.WMI I.llikt
itw-lMiniii T>lul>
9
W
n =
*
n
rtfOl
45
O»
CK
kurn
NW
n=44
PTI
CORPUS UTERI
9
W
n = 45
ft
lSlcnl lcrclcrcl
"" —«-m
NW
n =
|
^
CK
HCIM
44
t
CK
PROSTATE
g
W NW
n=45 n=44
ii
f*
CK
CK
a
1
CK
I
I
CK
rtmto
30
20
10
Figure 7.
Mean age-adjusted cancer mortalities in formaldehyde CPCs and
non-CPCs. (continued)
14
-------
I 200
UJ
ctw
CO
UJ
iiso
O
E
LU
= 100
to
i
so
TOTAL CANCER
o» 9
W NW W NW
n = 45 n = 44
5
5 2
*rii T
i-
T(
CPC
T
•5
1*1
CK
n = 45 n = 44
S5
1
pi-
£f
•i
CK
.t
M
CK
i
t.
CK
LARGE INTESTINE
l«rrt.M>|CM>
Figure 7.
W'WUK i . Mtat K Otomtf
•W-ltaWUtt I-SUMUIirtw
MB
Hna riiirti biAciM ihm tan
Mean age-adjusted cancer mortalities in formaldehyde CPCs and
non-CPCs.
,
ce
i
^
z
S
i
C9
£ 10
s
0*
W
n =
i
*
:K
"
1
CK
LIVER
9
NW W NW
n
1
CK
= 10
l-»
rii
CK
n = ll n =
!? 6
1*1*1 rli
S •* S
CK.Chnldl PnlKlii Cwd)
10
A
CK
STOMACH
o- 9
W NW W
n = ll n = 10
0
5
s
i
W
if « s.
CK
n = ll
i §
(gJ|CK|
NW
n
i
CK
W'WWi «.Htf»«tKI»urTil»u
00
0
IS
1]
CK
LEUKEMIA-ALEUKEMJA
0* 9
W NW W NW
n = 11 n = 10
ild
n = 11 n = 10
00
| 3 g
Cn 1 »
m
IcR '<"[ lcKlMl IS crc I5tltfcl
25
Hot nMl WlaM ttm Un
Figure 8. Mean age-adjusted cancer mortalities in carbon tetrachloride CPCs
and non-CPCs. (continued)
15
-------
200
ISO
100
50
TOTAL CANCER
o" 9
W NW W NW
n = 11 n = 10
S 5
I
JL
T
FK
*
crc
i
i*
crc
r-=
i
CK
n = 11 n = 10
i
1
ri-
CK_
I
CK
§
[1
crc
*|
CK
LARGE INTESTINE
0* 9
W NW W NW
• -11 n.10
1 i
1
CK
1
CK
CK
S
CK
n = 1l n = 10
S
to
S
•i
CK
*
CK
g
CK
ill
m
W
n-
1
ft
Mi
CK
11
in
rli
CK
RECTUM
0* 9
NW W NW
D-
|
left
10
8
h
CK
n = 11 n = 10
11 1 1
S crc |c5 «
CPC.CH.talPr.fcdi>, (tot, W.WMtt
•ONCPC.lm-amlalPnfedagtaialy «*.««wwti
> = UMn « OUtryittan
J.
nnimiKI I n
ESOPHAGUS
0* 9
W NW W NW
n =
i
evi
5-
CK
11
g
en
n = 10
S |
CK
A
CK
n = 11 n = 10
C3
s 5
fsi^lisf"1!
LUNGS
0* 9
W NW W
n = 1l n = 10
8 j g
1
CK
crc
m
CK
S
CK
n = ll
t S
m
Is {'"I
NW
R-10
i 1
Tl
si"!
BREAST
9
W NW
o = 11 n«10
1 =
[t
CFf
CK
1
CK
S
i
CK
CORPUS UTERI
W * NW
n = 11 n = 10
gill
jTlf
IS 1 m 1 1 S tre
§
25
CPC-omairrKid>|CiM|
W-WUtt
«W • In WHIM
Hun nlm MlaM itm Mn
Figure 8. Mean age-adjusted cancer mortalities in carbon tetrachloride CPCs
and non-CPCs.
16
-------
p
i
s
UJ
s
TETRAETHYL
LEAD
W NW
n = 6
i
li
s
§
ll
crc
crc
\
crc
PHENOL
9
W NW
n = 11
S —
1
rl
crc
I
crc
A
CK
ft
crc
ETHANOL
W NW
n=5 n-4
!
§
11 "
f¥i
•M
crc
'TrT '
, p
o
5
« crc
BENZENE
W NW
!
[1
crc
n = 28
T
8
1
r*i
crc ft
1
15
i
c **
CHLOROFORM
W NW
n = 6 n =
5
S 1
*"•; O
ITI
5 •*
crc
5
§
crc
CARBON
TETRACHLORIOE
9
W NW
n
i
n
crc
= 11 n = 10
1
*
crc
1
m
1
crc
50
25
CPC>CtMlcilrrMKlii|Cl>«l
«0« CPC • ««i-Chnlcll PrUntliit C«oi«T
W.WHB
IIW • »• Wtlu
Hail nhn MatM itm bin
Figure 9. Mean age-adjusted cervix uteri cancer mortalities in CPCs and
non-CPCs.
oe
UJ
8
Zi
GC
C3
£
OC
ts
CJ
0
UJ
I10
C9
TETRAETHYL LEAD
0* 9
W NW W NW
n = 6
1
C*C
^
[l|
crc
CD
0»
crc
I
1]
crc
n = 6
1
crc
ib
*
crc
1
crc
i
I
foe
0*
W NW
n = 11
C
a
1
1
crc
[i.
ere
1
crc
PHENOL
9
W NW
0
»
V
crc
Crx-ciiMiciiPndKi«gCMiT w.wwa B.
iilHicrc-itotauiciiriiociiiCiaiT iw-townti T
n = H
£
J
crc
1
crc
I
crc
-
crc
MwlMf ri Obnrvtttoa
ETHANOL
a- ?
W NW W NW
n=5 n=4
S
i ts
1
crc
*
CK
CM
]
L
K ***
n=5 n=4
2
i
crc
ft
crc
esj
rl
c*c
*S
J
crc
.ton.mMaMM.ln
Figure '10. Mean age-adjusted large intestine cancer mortalities in CPCs and
non-CPCs.
17
-------
s
£
CO
!S
i 10
!D CANCER MOi
OB
P 6
09
s
|
i 4
2
TETRAETNYL LEAD
O" 9
W NW W
n = 6
a s
r-
i
f
crc
3
I
crc
crc
n
CK
i
crc_
n =
i
ere|
NW
6
4
CK
rli
CK
PHENOL
0* 9
W NW W NW
n.ll
1
1
r>
•
8
ct
ft
CK
CK
1
1
crc
n = ll
18 S 2 ~
I5I"'I ISI01'
ETHANOL
o- ?
W NW W NW
n-S n=4
01
crc
§
§
S
II
<*• 5
1 crc
n = 5 n=4
l!
iiljt
1 5 1 m \ ere | »"
CPC'dolol Pnftclil (Mr
«OI CPC • M^cmicii rrifccm CHUT
I • taMr it Otommu
I-
Figure 11.
Mean age-adjusted esophageal cancer mortalities in CPCs and
non-CPCs .
£
a.
220
|
ffi
U
i
2
BREAST
9
W NW
n=5 n=4
Si
n
S
{3
crc
1}
CK
i
CK
CERVIX UTER
9
W NW
n=5 n=4
S
n
s
S
s
r- •
§
t-;
i, •••
±
crc ^ a
LIVER
_» Q
Cf t
W NW W NW
n=S n=4
3
!
T
rn
T
* «
«M> mm
M
s
_
ere
n
n
J
i
crc
n=5 n=4
tloMiimtiii
1
^ W 5
fn *i
S crc 5 CfC
-Owtal Pirtnui Cmn
MHCPC-iUH>uialPiMKliiCiaiy
Figure 12. Mean age-adjusted cancer mortalities in ethanol CPCs and non-CPCs.
18
-------
s
i
w
1
ii
m
n
3
iri
*
CfC
LIVER
0*
NW W
= 11
*.—
1
s_L
r^
1
crc
i
CK
9
NW
n = 11
aMU
1
rt
CK
kml
f
fii
crc
nn
1!
e-J
1 CK
f
rn
crc
CORPUS UTERI
9
W NW
1
ill
PC
n
s
•fn
ere
= 11
i
S
f
™
n
CK
BREAST
9
W NW
n-11
1
I
rt
Pf
*
CK
PC
I
crc
20
10
i.krjkviiatiKYMtai
Figure 13. Mean age-adjusted cancer mortalities for phenol CPCs and non-CPCs,
|
TETRAETHYL LEAD
0* 9
W NW W NW
n = 6
8
I
m
S
f
CK
1
crc
1
CK
n = 6
8
^
|t
n
8
era
fl
S?
1
crc
PHENOL
0* 9
W NW W NW
n = 11
R
ai
crc
•£1
CK
i
pf
fl
CK
n = 11
r*
PC
CK
f
n
i
•
9
CK
ETHANOL
0» 9
W NW W NW
n=S n=4
is
{
CfC
}]
CK
5
CK
a
i
CK
n=S n=4
f*
CK
1
CK
§
*
55
i
ere
CPC • CkHttal Pn*cm OM)
m crc.
H'fkiWUli T.StutMt
•m nlm Miaul tfm kn
Figur.6 14. Mean age-adjusted leukemia/aleukemia mortalities for CPCs and
non-CPCs.
19
-------
s
LARGE INTESTINE
n» 9
W NW W NW
n = 6 n-5
1
2
il
t
iff
*
CK
S. "
n-6 n=5
T
i
CM
s s
i
Cff
ri
*
CK
1
crc
T
•
crc
CERVIX UTERI
9
W NW
n = 6 n=5
a
is
2
CK
1
o r
1*
e»
•
!
{
»c ere
BREAST
9
W NW
n = 6 n = 5
1
§
CM
§
T
It
m
Fl
crc
i
'
i
« ***
TOTAL CANCER
o" 9
W NW W NW
n=6 n=5
si .
g
T
i
gK_
CK
1
tit _.
ere EPC
n=6 n=5
S §
I
pf
crc
1
i
crc
ft
IfK
CK
zoo
100
W.WUU
r -
I CK
s§s
lsl«l 15
= 5
I
CK
RECTAL
d- 9
W NW W NW
n-6 n=5
1
CK
1
CK
|5
7
CK
n=6 n=5
Ml
crp_ *" lac w*
CK •Onlal PraiMii C**l
UK ere • IM-OralcH PiMKlii t
•W'lMwui I.taxrtt
mm MtaM ttm tan
Figure 15. Mean age-adjusted cancer mortalities in chloroform CPCs and
non-CPCs.
20
-------
§
2
CE
O_
£20
AGE-ADJUSTED CANCER MORTAL
O
LARGE INTESTINE
d- 9
W NW W NW
n = 28
00
-
I
•n
ere
5
i
CPC
•
m
CPC
1
i
CPC
n = 28
c4
rl
•m
CPC
i-
CPC
M7
C*i
1
vc
I
rj
1
we
CERVIX UTERI
9
W NW
rt
IPC
n = 28
T
8
CM
i
f*l
CfC
PC
to
i
BREAST
9
W NW
n=28 n = 28
S3
CO
rl
X
CPC| |gj|cpc
a
to
1
1
ISM"1!
TOTAL CANCER
CMilcil Praduting Cmlr
KOHCPC.Km.CM.lc.IPr.IKlnsC.nitr
W • Wwti
HW-KooWWl
n = Hgibu ll ObnmUmt
I .SBnUirt m.
Hun vilms Imllcitid ibtn bin
s
0
I
i
ESOPHAGUS
o- 9
W NW W NW
s
<4
i
CK
n = 28
«O
s
(O
I
CPC
CPf
ft
CPC
n = 28
^
rnlTl
l«i«lis[«
LEUKEMIA ALEUKEMIA
HOI ere • Hn-Clinlal Mfedit Cinuy
n > Muab«f it OburvillMi
•in nlni MleUM ibm bm
Figure 16. Mean age-adjusted cancer mortalities in benzene CPCs and non-CPCs.
21
-------
g
s
PHENOL
O*
W NW
n = 11
o>
!•
*
IS.
10
i
CPC
i
I
en
CSI
• -I
CPC
TETRAETHYL LEAD
0*
W NW
n = 6
S
9
S
if
2 -r
CPC
T
CK
CPC • tMlal PndKtai Cintl
KOI CFOtoOMIciJ PndDdM CMtt
crc
CK
ETHANOL
0*
W NW
n=5 n=4
S!
i
CPC
*
:rc
W-WUK
••
S
s
C*J
CM
- 1
•L
CK
IllOI
T.u
BENZENE
O*"
W NW
n = 28
N
OJ
i!
ri
CfC
*
CPC
J-
CPC
1
t
crc
CHLOROFORM
0*
W NW
n=B n=5
i
11
*
CPC
CPC
1—
CPC
§
M
1
•
CK
CARBON
TETRACHLORIDE
0»
W NW
n=ll n = 10
11
i
£ n
il
« cft
•
CPC
rt
CK
IMT •( ObsamtiMi
Una vtlun IndlctM ibm bin
Figure 17. Mean age-adjusted prostate cancer mortalities in CPCs and non-
CPCs.
i
s
UJ
Q_
CO
STED CANCER MORTALITIE
§
3 100
TETBAETHYL LEAD
- O
CF T
W NW W NW
n = 6
5
§
f«-
i
Mi
CPC
S3
1
CPC
1
i-
Cf
d>
it
CPC
n = B
rd
Mi
M
S
~
CK
i
ii
CPC
ii
CPC
PHENOL
0" 9
W NW W NW
n = 11
I
oa
ri
CPC
§
CO
CPC
1
CPC
a
i
CPC
n = 11
111
rip 2
'"
CK
[i
CfC,
rii
CPC
ETHANOL
o* 9
W NW W NW
n=5 n=4
1
frt
i
CK
S
I
CK
1
CK
n=5 n=4
Irlri
r±
CPt
CK
^
I
CK
crc •anim tntnot, CMH
mi CPC • Mt
a . IMtir U Otunnha
•ill nun liXlalM itan btt
Figure 18. Mean age-adjusted total cancer mortalities in CPCs and non-CPCs.
22
-------
0
v>
UJ
^
«
0
E
S
5
ft 10
i—
AGE-ADJUS
BENZENE
0" ?
W NW W
s
1-
m
n = 28
§
10
CK ,
•p
is
.1]
5 CPC
1
f*
CPf
n
ii
CK
= 28
3
ni
1™
NW
1
CPC
CHLOROFORM
W NW W
n
§
CK
= 6 n =
S =
~ s
in i!
I]'
CK ;
5
<
9
* «
n = 6
1
CPC
to
CK
NW
n
1 CK
= 5
i
C*3
CK
FORMALDEHYDE
_ 9
W NW W NW
"
&
rl
•M
CPC
= 45 n = 44
s
__ !J
CB
i
CK
if
CPC
•
crc
n = 45 n = 44
If 11
T T T T
$
Mi ,„ MM ,„
CK trv CK CPC
CK •Ctnliil PndKUg C«nli
»ONCre.H«-a».lcilPr,Ii«.gC«iit| >W.H|BW.IU
Hat nl«n ladlattd itm tan
Figure 19. Mean age-adjusted liver cancer mortalities in CPCs and non-CPCs,
23
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REFERENCES
1. Fairchild, Edward J., Richard J. Lewis, Sr., Rodger L Tatken, Eds.
Registry of Toxic Effects of Chemical Substances, Vols. I & II.
Cincinnati, OH. DHEW Pub. No. (NIOSH) 78-104-A, 78-104-B, September
1977. 930, 987 pp.
2. Garner, D. N. and P. S. Dzierlenga. Organic Chemical Producers' Data
Base Program, Vol. II. Radian Corporation, Austin, TX. 1976.
3. Hoover, Robert, Thomas J. Mason, Frank W. McKay, Joseph F. Fraumeni, Jr.
Cancer by County: New Resource for Etiologic Clues. Science 189:
1005-1007. 1975.
4. Hoover, Robert and J. F. Fraumeni. Cancer Mortality in U.S. Counties
with Chemical Industries. Environ. Res. 9^:196-207. 1975.
5. Kwalick, D. S., W. Halperin, R. Altman, M. Goldfield, J. E. Finley.
Cancer in New Jersey: The Problem and Solution. J. Med. Soc. of
New Jersey 73(10);869-880. October 1976.
6. Levin, David L., Susan S. Devesa, J. David Godwin II, Debra T. Silverman.
Cancer Rates and Risks. DHEW Pub. No. (NIOSH) 75-691 (2nd ed.). 1974.
7. Mason, Thomas J. Cancer Mortality in U.S. Counties with Plastics and
Related Industries. Environ. Health Perspectives.
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TECHNICAL REPORT DATA
(Please read Instructions on the reverse before completing)
1. REPORT NO.
EPA-600/1-79-022
2.
3. RECIPIENT'S ACCESSION NO.
4. TITLE AND SUBTITLE
PRELIMINARY ANALYSIS OF CANCER RATES IN ORGANIC
CHEMICAL-PRODUCING COUNTIES
5. REPORT DATE
June 1979
6. PERFORMING ORGANIZATION CODE
7. AUTHOR(S)
Amy J. Cross and G. Bruce Wiersma
8. PERFORMING ORGANIZATION REPORT NO
9. PERFORMING ORGANIZATION NAME AND ADDRESS
Environmental Monitoring and Support Laboratory
Office of Research and Development
U.S. Environmental Protection Agency
Las Vegas, NV 89114
10. PROGRAM ELEMENT NO.
1HE775
11. CONTRACT/GRANT NO.
12. SPONSORING AGENCY NAME AND ADDRESS
U.S. Environmental Protection Agency-Las Vegas, NV
Office of Research and Development
Environmental Monitoring and Support Laboratory
Las Vegas, NV 89114
13. TYPE OF REPORT AND PERIOD COVERED
Final
14. SPONSORING AGENCY CODE
EPA/600/07
15. SUPPLEMENTARY NOTES
16. ABSTRACT
This study is designed to determine whether there is an association between cancer
mortality and the production of environmental carcinogens. Mortality rates of
counties containing organic chemical production facilities are compared to rates
of control counties. Twelve different cancer sites in lung, stomach, etc., and
eight organic carcinogens were considered. Although a rigorous statistical analysis
was not conducted, for most cancer sites mortality rates were found to be higher
in counties of osganic carcinogen production than in control counties. The study
aids in the development of statistical techniques for determining the contribution
of environmental contaminants to the rise in cancer rates. Research of this type
assists in the identification of compounds that need to be regulated.
7.
KEY WORDS AND DOCUMENT ANALYSIS
DESCRIPTORS
b.lDENTIFIERS/OPEN ENDED TERMS
c. COSATI Field/Group
carcinogens
epidemiology
mortality rate
ecology
demography-
organic chemical manu-
facturing sites
site-specific cancers
68, G
05, K
57, H
18. DISTRIBUTION STATEMENT
RELEASE TO PUBLIC
19. SECURITY CLASS (This Report)
UNCLASSIFIED
21. NO. OF PAGES
32
20. SECURITY CLASS (Thispage)
UNCLASSIFIED
22. PRICE
A03
EPA Form 2220-1 (Rev. 4-77) PREVIOUS EDITION is OBSOLETE
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