&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

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                                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

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                                  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

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                                   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

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                               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).

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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

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Figure 2.
Counties of significantly high trachea, bronchus, and lung cancer
mortalities 1950-1969.

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     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

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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)

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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)

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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)

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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

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 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

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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
—
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a a
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a

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5

BENZENE
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n = 28
m
1
s



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ri •»
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8
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n =








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±1
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CHLOROFORM
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n = 6 n = 5'

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ll

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ft

CK 55 C
f n = 6 n
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= 5


UH nlon MlaM iMn kin





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40

i M
UJ
| 30
1,

2 ;n
f?. 20
i
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10

TETRAETHYL LEAD
o- 9
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n = 6

1

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rf






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E
rin
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n = 6






s §

g
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0" 9
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n = ll



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J.



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PI
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1
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rt
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n =








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11








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rn

CK
ETHANOL
o- 9
W NW W NW
n=5 n=4

ri
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a »
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n
n


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crc CPE
n=5 n=4





S
— 40
rfi?
5 g Tl
T T
T*
CK « JR. tK
               cn •OMitii rnmcui c««r
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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
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...


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



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4
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n


CO
I
fl
crc
NW
-11


i
crc
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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_ "
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CK
~
to
CPC
n


J
CK
•on nlm IKIcitM iMn bin
= 5



cn

NW
n=4


1
ere



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CK














Figure 6.  Mean age-adjusted rectal cancer mortalities in CPCs and non-CPCs.




                                     13

-------
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       oe
       UJ
       Q_



       S



       *


w
n=45


3 *

Wf wc
•01 ere
ESOPHAGUS
d* 9
NW W NW
n=44


1

CK
ft

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n = 45 n = 44



§i IS
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LUNGS
o» 9
W NW W NW
n=45 n=44
| s
I


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•£|


CK
|
CO


5
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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


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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




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.t




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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
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1
CK


LIVER
9


NW W NW
n






1
CK
= 10






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n = ll n =






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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]
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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
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crc
i
i*


crc
r-=
i



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n = 11 n = 10

i
1
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[1


crc
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LARGE INTESTINE
0* 9
W NW W NW
• -11 n.10

1 i
1


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1


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S


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n = 1l n = 10

S
to
S
•i


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*


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g


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ill


m
W
n-




1
ft
Mi
CK
11



in
rli
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RECTUM
0* 9
NW W NW
D-




|
left
10



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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 =



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evi
5-
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11



g

en
n = 10


S |


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A

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n = 11 n = 10



C3
s 5

fsi^lisf"1!
LUNGS
0* 9
W NW W
n = 1l n = 10
8 j g
1



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crc
m



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S



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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


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1



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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







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§

11 "
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5




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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
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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>
•


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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
§



§



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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^
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i

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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
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§
*
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
*
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1
crc

T


•
crc
CERVIX UTERI
9
W NW
n = 6 n=5



a
is

2
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1
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{

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BREAST
9
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n = 6 n = 5
1
§
CM
§
T
It

m

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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
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ft
IfK

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                                                                              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
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|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

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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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