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APPENDIX II The Magnitude of the Industrial Chemical Cancer Problem: A
Review of Some Opinions and Numbers*
Richard Wilson ,, Department of Physics
and Energy and Environmental Policy Center
Harvard University Cambridge, MA 02138 II.1. Introduction It has been stated in the public press and sometimes with the names of distinguished scientists attached, that the chemical industry could be the cause of most of our cancers. I think this is exaggerated. The origin of this view is probably the calculation that 80%-90% of cancers are environmentally caused; from a statement that they are environmentally caused to being caused by chemicals in the environment is a small step--and quite likely to be cor rect. The further step that these cancers are caused by explicit and direct actions by the chemical industry is a larger one and one which is far less likely and cannot now be proven.^- Indeed, there
is negative evidence that it is not true;'no one has derived this large a number directly.
On the contrary, it is probable that much of this number is due to dietary habits and individual preferences--such as a choice to drink alcohol and to smoke cigarettes--the last of which is well
**
known to cause 40% of all cancers.
Originally written as a separate report. **This is actually the fraction for men. Present exposure for women
approaches that for men, so that the figure for women is expected to reach this percentage soon.
i
AP00008990
t
These points are brought out in several review articles. 2--7
97
ZZ.2. The proof that cancer is environmentally caused Inbred strains of rodents differ significantly in their sus
ceptibility to induced and spontaneous tumors and this led to the belief that genetic factors might also be of major importance in man. Apart from the obvious advantage of skin pigmentation in preventing skin cancer caused by ultraviolet light, and a few other exceptional cases this is no longer widely believed.
Firstly, it has been shown that as men migrate from one country to another, they assume the cancer patterns of the host country rather than those of the country of origin. Secondly, where strong carcinogenic effects have been observed in man--smoking causing lung cancer, chemicals causing bladder'cancer--attempts have been made to find a genetic susceptibility but none has been found.
Zf we then assume that cancers are environmental in origin, we might try to reduce the cancer risk to that in the country with the lowest risk, or better still, to construct a life-style whereby each and every cancer has the lowest risk of any that is observed in any country. When we do these comparisons between countries, we must correct for the fact that the major observed determinant, .of cancer is age, and compare only age adjusted cancer risks.
p Higginson for example calculated the lowest rate of. any one site between the African Bantu and the United States. Thus for liver cancer the U.S. incidence was chosen because the Bantu have
i
AP00008991
98
a high rate of liver cancer--due possibly to a high level of
aflatoxin B in their diet--and the U.S. has a relatively lower
rate. On the other hand, the U.S. has a high risk of lung can
cer among males--due probably to cigarette smoking--so in this
case the lower Bantu figure was chosen. By this means tiigginson
argued that a hypothetical country could have a cancer risk as
little as 10-20% of the present level..
This argument has been accepted by most reviewers on cancer.
The reviews of Higginson, Doll, and Wynder and Cori, all outline
this procedure. The exercise is now much easier than 20 years
ago because there exist several good cancer registries.'
11
We must recognize the various sources of our data on cancer incidence in man. These come mostly from iatrogenic and occupational causes. Tables II-l, 11-2, IX-3, XI-4 from Doll12 show the sources
of essentially all our detailed information. Since occupational
cancers are a large source of our information, naive people might
be excused for thinking that occupational cancers can be & large
source of the cancers. But this logic would suggest that since
iatrogenic cancers are a large source of our information, that
doctors are a large source of the cancers> Higginson and Muir
of the international Agency for Research on Cancer state:
"Although occupational cancers recognized so far provide some of the most satisfactory data for identifying external*' agents, the absolute number of cancers due to occupational exposures would appear to be relatively small, probably 1% to 3% of all cancers. To what extent low levels of exposure to industrial carcinogens in the general population contri bute to the overall cancer pattern remains a matter for speculation."
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I-IX am
Table Z1.3
Table 6 Occupational causes of cancer contributing lo general environmental pollution
Agent
Site or cancer
lontiing radiations
Polycyclic hydrocarbons
in sool, ur. and oil
Arsenic
Asbestos '
Vinyl chloride
Bronchus Skin Hone Marrow (leukaemia) Skin, scrotum
Bronchus Skin
Bronchus Bronchus Pleura, peritoneum
Uver (angiosarcoma)
100
Table 11.4
Tabic 7 Ollier environmental cam** of cancer
*Asr
Site of ejneer
Sunlight Associated with we of'Kanjri' *nd `dhoti* Reverie smoking' Chewing betel, tobacco, lime Smoking Afl.xtuxin SehistoSOmlaxix
Associated with sexual intercourse
C*pu!
(rotten! ulcer, miMtiMm carcinoma. ? melanoma)
Skin of abdomen, groin, and thiph (squamous carcinoma)
Palate
Mouth
*
Mouth, pharynx, larynx, bronchus, Oesophagus. bladder, 7 pancreas
Liver
Madder
Cervix uteri
I
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I concur in this, but now follow the speculation. One of the useful sources for speculation are the geographical distri butions of cancer mortality. Another source of speculation is the listing of chemicals in the water supply and estimates of their carcinogenicity from animal data.
This set of speculations is' not complete, but is intended to
suggest a logic and to point out some of the major carcinogenic risks in the environment.
In this speculation I make distinctions between voluntary risks, cigarette smoking, drinking of diet sodas, and involuntary risks, such as exposure to air pollution. I also distinguish be tween those chemical risks--such as aflatoxin B in milk and nuts, and even chloroform in water13--which are naturally caused and
those which axe caused directly and indirectly J^y the chemical industry--food additives, air pollution, etc".
1 follow human data whenever possible, thereby avoiding the uncertainties on extrapolation of animal data to man stressed by Epstein.
11.3. Arsenical cancer 14
This has been studied by Blot and Fraumeni.
They find an
increase in lung cancer in U.S. counties where there is copper,
lead, or zinc smelting. The increase, demographically corrected,
is 17% for males and 15% for females. They attribute this to
arsenic from the smelting- operations.
No absolute numbers are given in the paper for reference 3
AP00008995
102
so derive these as follows; this leads perhaps to an overestimate. These 36 counties were 1:2% of U.S. counties. The 71 counties,
including all smelting and refining (including non-ferrous bres with little arsen% ic) employed 50,000 persons in smelting. About half of these were presumably in the ferrous industries and these were 1% of the total population. The population at risk was then about 2.5 million (this is 1.2% of U.S. population in rough agree ment with 1.2% of U.S. counties!).
The normal lung cancer incidence was (1950-68) 38/100,000 among males and 6/100,000 among females and has since risen (due pro bably to cigarette smoking) The increase due to arsenic becomes
' rro * roo3,Vd * i/25ofooo
1,250,000'= i + 11 -
92/year I multiply by 2 to allow for the fact that in cancer about as many cancers may be caused in other sites than the principal one. I multiply by 2 to allow for spread of arsenic beyond the
borders of the counties discussed to get 360 cancers/year caused by arsenic.
The male/female difference is probably a synergism with ciga rette smoking and an extreme industry advocate could attribute. most of them to ciagrette smoking. In situations like this where
**
there is a multiple cause, it seems fairer to ascribe half to each cause.
>
AP00008996
103
II.4. Benzene The recent OSHA hearing shows that the leukemia rates from
benzene exposure used to be large in some European countries. Kith present U.S. standards the calculations suggest a leukemia rate in the U.S. of less than 1 per year15 due to benzene exposure.
II.5. Vinyl chloride Vinyl chloride cancers seem to have caught public attention
more than any other. They, once diagnosed, are particularly easy to assign to vinyl chloride because liver angiosarcoma is rare. .
So far, worldwide, 65 cases of liver angiosarcoma hav^ been
#
diagnosed among.vinyl chloride workers. They were attributed to the large exposures prevalent until recently.
If we allow for a latency period, we mightexpect 40 more to be "in the pipeline." Moreover, there afe two studies1' ^
which suggest, but don't prove, since it is not statistically signigicant, an equal number of cancers at other sites. This suggestion is also consistent with statistically significant data on rats. Therefore, I suggest that there may be a total of 150200 vinyl chloride cancers worldwide to date among 1,000 workers
2
exposed heavily at least 10 years. This was a risk of 2 x 10 / year, now much reduced'. Allowing for cancers at other sites, and others not exposed occupationally, we might reach 200/year. The number must now be reduced a factor of nearly 1000 by reduced occupational exposure to .less than 1/year.
t
i
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It is interesting that in a brief, non-random, sample of my colleagues in pure science, all of them thought, in advance of my calculation, that there were many vinyl chloride cancers a year; those that guessed a number thought 1000/year, This is an effect of alarmist newspaper reporting.
II.6. Asbestos
There are two major authorities on asbestos cancers: sir
Richard Doll and Dr. I. Selikoff. From Table 2 of a review article by^elikoff
-----
we note that
the cancer risk from asbestos is large only among cigarette smokers
where the risk of lung cancer is multiplied by 5.7. There are
200,000 workers in the asbestos trades, 80,000 having left it,
half of whom presumably smoke. Partially dicounting those who
left the trade, I estimate 200,000 workers at risk with a yearly
risk of lung cancer as (5.7 - 1) x 1.2 x 10"3 *= 6 x 10-3
giving a total number of lung cancers of 1200/year. This has pro bably been reduced now, by care in the workplace, about a factor of 10,
The maximum concentration that has been found at building sites where asbestos was being sprayed is 1000 times less thanthat in the asbestos industry, which is about 0.1 mg/m3 and was'-pro- -
bably more in the days when workers got lung cancer and the aver
age concentration in towns is 100 times less than that in the asbestos industry. 19
If I assume proportionality I derive an upper limit to risk
AP00008998
105-
around building sites of less than 6 x 10~6/year and in the ordinary town environment of 6 x 10 /year leading to at most 12 cancers/ year in the U.S.
II.7. Uranium miners It is now well known that uranium miners have developed can*
cers. In the U.S. there is a survey by Lundin. 20 At that time 60 lung cancers had been observed# 58 among smokers, versus 15 expected among smokers in the general population. Only two cancers were observed among non-srookers. Because of this synergism, we could blame most of the effect on cigarette smoking and little on the mining. However, if we blame it all on the mining, and in clude more recent cases# we find about 20 cases/year over the whole U.S. This number is now reduced due to increased precautions.
We can take this as an indication--one of many--of the carcino genic effect of radiation. Assuming proportionality, I find 3000 cases/year from natural background radiation, a similar number from diagnostic x-rays, but very few from industry.
II.8. Worst case estimates
Instead of trying to get numbers from each industry, one can
start at the other end and see if in some geographical areas there
is more cancer than others that can be attributed to a chemical
cause.
A
start
on
this
for
the
U.S.
was made
by
Hoover
a*n' d
21 Fraumeni
using the Atlas of Cancer mortality previously noted. They note
t
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4106
that for cancer at three organs--bladder, liver and lung--the
mortality rate is higher in areas with a chemical industry. The
worst case# then, is to assume that this increase is due to in
dustry and probably occupational.since the increase is primarily
among men. We must, however# note that these cancers are in the
1950-69 period and probably based on exposures in the 1940-1960
period which were probably worse than now.
If I nonetheless make the extreme assumption that the male/
female difference is all due to this industrial effect# 1 find
the increased rate of bladder cancer among white males is 6.78 -
22
2.39 * 4.39 per 100,000 per year or 4#4Q0 cases per-year.
But
.this does not allow for the fact cigarette smoking causes bladder
cancer and for the years in question there was a large male/female
difference in lung cancers due to the later introduction, of the
smoking habit among women. Therefore, I reduce this to 2#200
cases/year.
Hoover and Fraumeni find a smaller difference# of 0.41 per
100#000 per year in chemical industry counties. With 864#542
chemical workers (in 1960) this difference is 3.5 cancers/year.
My figure is therefore much more pessimistic. We should not
allow for an equal number of cancers at other sites since I am
calculating these separately. This large fractional increase in bladder cancer for some
counties in New Jersey has led to dramatic newspaper headlines. However# a detailed study by Dr. Demopoulous23 of N.Y.U. Medical
Center shows (in much more detail than I) that firstly it is not
t
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t 2-07
proven that the cancers are caused by industry, and secondly, that even if they are the number cannot be great. Ke claims that, no more than 00 of the 14,000 cancer deaths in New Jersey (4.3%) could be industry related, and. in most of these cases the industry could not be wholly responsible. The number of cases for which industry is solely responsible (i.e# no attribution to cigarette smoking) is 1%. I note that this is. the "worst" county according to a casual study of the U.S. Cancer Atlas.
II.9. Worst case estimates for a specific organ--bladder Bladder cancer is a good example. Cancer of the bladder might
be expected as the body endeavors to excrete an unusual load of toxic chemicals. Beta napthylamine and benzidine in particular in creases the risk of bladder cancer.^ The authors note that of 21 counties in New Jersey, 18 have bladder cancer rates in the high est decile of all white male rats, whereas white females do not.* This male/female difference is indicative but not proof of an occupational hazard in the chemical (petrochemical) petroleum industrial complex in the area.
But we must be cautious at assigning this to the chemical industry. The effect in Los Angeles county is almost as big. .This suggests that a large part could be from carcinogens in automobile exhaust since L.A. has very little chemical industry.
i
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108
XI.10. Worst case eBtimates--liver and kidney cancers Another type of cancer that night be related to chemical
carcinogens is liver or kidney cancer. Many of the industrial
%
chemicals which are carcinogenic in animals give liver or kidney cancers as these seem to be the organs where the metabolites are formed*
Here, however, it is hard to point to an occupational origin. In the years 1950-69 there were 76,070 deaths from liver and bi liary cancers among white males and 94,229 among white females. There is & tendency to concentrate in areas of chemical industry. It would be hard to attribute more than 10% of these male cancers to occupation--!,000 in 20 years or 350 maximum per year. Hoover and Fraumeni find a difference between chemical industry counties or 0.46 per 100,000 for men and 0.24 per 100,000 for women. Among the chemical workers this is 3/year for men and 1.5 per year for wcfcnen. Again my numbers are much more pessimistic. The 1.5 per year could be taken as an indication of environmental cancers.
For the kidney there is a male/female difference: 57,780 among male whites and 34,204 among females. If the difference is all occupational, this leads to 1,000/year and again allowing a factor of 2 for other sites, X find 2,000/year maximum although I find here no particular excess in areas with chemical industry. The % liver cancers might all be due to aflatoxin In the diet and a rea sonable calculation suggests that at least one tenth of them are.
Assuming liver cancer incidence data from southeast Asia
i
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Africa, and the U.S. concentrations of aflatoxin in peanut butter
and milk,
1
calculate
*
a yearly
liver cancer risk of
10--5
for
four
tablespoonfuls of peanut butter a day or 4 pints of milk a day.
The actual consumption of each is about 1/6 of this, so the over-
all risk from aflatoxin in the diet is about-3 x 10 /year on a
strictly proportionate basis. This leads to 2 x 10 x 3 x 10 *=
600 cases per year in the U.S. population. This is one tenth of
the total U.S. liver cancer mortality of 8,500 per year.
II.ll. Worst case estimates--lung cancer It has been noted that blue collar workers smoke cigarettes
more than white collar workers. It is true that blue collar workers get more lung cancer than white collar workers? this is usually attributed to smoking but it has been claimed that it is due to occupational effects of all sorts. fjoover and Fraumeni find an excess of lung cancer of 3.8/100,000 among men in chemical industry counties (Table II.5 from reference 21).
However, if this claim were true, we would expect to see an excess of lung cancer among non-smokers in the occupational setting. Unfortunately, the U.S. Cancer Atlas cannot help us because this data is not recorded. There is no evidence that non-smokers ex posed to asbestos get lung cancer and although a few non-smoking uranium miners got lung cancer the effect is not large. If we take Hoover and Fraumeni's data as an upper limit, we find 320 lung cancers/year among workers in the chemical industry.
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11Q
Table II.5
Avrmu Amkual AOfAntvmp Moltmity R*tit amoxc Wnrrr ro* At l Malic?*anchi akb rod Canci m or Fm a Irtrtr ie Jittt n i in. Total U.5. *-r> im 139 Cmimicai-HOUSHYCOU.ntii.v(!9.'0I9S9J
mplttnt
Long
Site*
BUWer
Lier AnJ gnJIbUdJcr
Lattice
Me* Chemf(al-|itduUr)'(wiHiev Total tf.S. JUlio of racy ftiftctcncc hrtorcn iaic
tOm** Chrmical-imtnTtiy reunite*
Tvlrt MJa. Rntisef ratc Dilftttih'C fcflurrn w*t
m t' < OjOJ,
ITy.si 174 (M
1.0 5.77*
IJI/C 130.10
1.0 U2*
41.79 37.01
1.1 i.tr
t*s *.29 1.0 0.1*
7.** 1.7? 1.1 0.41*
.3.57 2.19 1.1 O.t**
s.a 5.1* 1.1 e.46*
1.0 * 0.24*
LI 1.1 .e
3-0 5.7 to -0.1
i
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Ill
We might have expected that the breathing through the lung is & way occupational cancers can be caused. However, apart from the specific occupational cases discussed/ none have been identified and the non-smoker's risk of lung cancer can be partially occupa tional. I take as an upper limit the difference between country and town and weight by the total urban population to find less than 1,000/year in the U.S.--more pessimistic"than Fraumeni's number.
11.12. Occupational chemicals as environmental cancers
We can ask ourselves, of the chemicals produced in the chemi
cal factories, how many of them give trouble in the environment?
If there were a threshold below which the chemicals cause no trouble,
this would not be a problem, but if there is a proportional effect
the large numbers of people exposed environmentally can outweigh
the low concentration.
The notes on asbestos above suggest that the difference in
exposure in the occupational setting and the environmental setting
is usually large and that for chemicals well controlled in the
workplace there is little environmental risk. But we can check
this by looking at the end points of the chemicals.
We can consider two sources of exposures
1) through the air
*
21 through the water
X consider them both below, using human data when possible
and animal data when not.
i
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IX.13. Water pollution
There is a recent National Academy of Sciences report on
Health Effects in Drinking Water?^'
This lists the carcino
gens found in drinking water and estimates risks for each one of them. In most cases the risks are based on animal data since the exposure is sufficiently low that there is no human data.
X enclose tables from these articles. I note that the high est risks are from chloroform--a carcinogen of moderate potency but present in high concentration in some places--and dieldrin. Dieldrin, a pesticide which is a potent carcinogen, is now banned and is present only in some drinking water. It represents there
fore only a local hazard.
The survey is not complete, but a rough average gives a risk of 5 x 10--8/year from chloroform in drinking water (giving liver
and kidney cancers) leading to 10 cases/year over the U.S. and
--8
perhaps as much as 10 /year or 1 case from dieldrin.
11.14. Air pollution 27
There is evidence that air pollution causes an increased
mortality rate of 30,000/year in the U.S. in 1977. This is often
attributed to sulphate particulates, but it is largely undifferen
tiated between nitrates, sulphate particulates, and trace elements.
*
Some of the trouble could be carcinogens--such as benzo (a) pyrene
which is a known animal carcinogen. Thus, in a study of cancer in Liverpool and N. Wales28 Stocks
i
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Table tl.6
national organics recokimssance soryet water quality oata
DATA FROM 80 UTILITIES FOR FOUR TRtHAlOMETIANES* CARSON TETRACHLORIDE, ANO 1,2-OlCHLOROCTHANE1
Utility Mate
(Plant Hjn:g when Applicable)
Chloroform *Q/1
Bromodichtoro* mjthane
VO/1
Olbromo* chloro* methane ufl/1
I. Lawrence Water Works
*0.1 91
*0.2 9
NF* 0.6
2. Waterbury Bureau of Water (Morris Treatment Station)
ItF OF OF 93 10 0.6
3. Metropolitan District Comission
(Norumbego Treatrent Station) Baton, Massachusetts
of Of OF 4 0.8 IIF
4. Newport Dept, of Water (South Pond Reservoir Treatment Plant /I]
of 103
OF OF 42 13
5. Department of Water Resources Mew Tork, Hew Tort
OF OF Iff
n ? 0.9
6. Puerto Rico Aqueduct and Sewer Auth. (Sergio Cuevas Water Treatment Plant)
*0.1 47
OF 29
OF 16
7. Passaic Valley Water Commission Little Falla, hew Jersey
0.J 59
,
OF 16
ItF 2
fl. Toms River Water Company
0.4 \ 0.6
OF <0.8
\
1. First line in Italics Is raw water data Second line In regular type is' finished water data.
2. nF - None Found 3. - Some raw water data may he in error because of incomplete-combustion
of particulates In some raw waters.
OF 3
flro*9
form wo/I
OF NF
OF <1
OF NF
OF 1
OF Hf
OF 2
OF NF
OF MF\
1
1.2-
Dlchloroethane *o/l
OF NF '
OF <0.2
OF NF
jrr NF
OF f
. OF NF
<0.8 <0.2
OF hf
Carbon Tetrj> chloride uo/1
Non*
Volatile Tatal Organics
Carbon
n/1
or 2.? NF f.6
OP 2.2 <2 2.9
OF 2.1 HF 2.0
OF d.d NF 4.1
OF J.0 NF 2.S
ft'F 2.0 NF 2.0
<2 J. <2 1.9
OF <0.05 NF <0.05
e 1? T**
4' 7S. V*.
H
H U>
p*. .
**
. (-1 v ..
J%
( Lj
Ct
U C-
. Utility Nine (Plant Rame When Applicable)
20. Huntington Water Corp.
21. Wheeling Water Department
22. Miami-Dade Water and Sewer Authority (Preston Plant)
23. Jacksonville Dept, of Public Works (Highlands Pimping Station)
24. Atlanta Waterworks (Chattahoochee Plant)
2S. Owensboro Municipal Utilities'
26. Greenville Water Oeparurent
27. Tennessee American Water Company Chattanooga, Tennessee
26. Memphis Light* Gas and Water Oiv. (Malloy Plant)
29. Metropolitan Water and Sewerage Oept, (Lawrence Plant)
30. Commissioners of Public Works (Stoney Plant) Charleston* South Carolina
Chloroform 1
'1 23
0.9
n
KF 311
ttr
9
<0.1 36 .
KP U
0.3 U
0.9 30
<0.2 0.9
0.1 16
<0.9 )95
Brcmodichloro* methane
lo/I
Dibromo* chloro* methane
KF 16
LT 26
nr n
KF 4
KF 10
KF 20
nr 6
KF 9
KF '2
KF S
KF 9
OF S
KF 17
" KF". 35
KF 2
MF 2
KF 17
KF 3
KF 0.7
NT 1
KP *0.9 .
OF 0.6
Brono* form wQ/l
KF hr
KF Of
KF' 3
KF W
KF NF
KF 3
KP <1
KF NF
KF NF
KF HF
KF 0.8
1.2* Oichloro*
ethane s.C/1
Carbon Tetra* chloride *.0/1
Non*
Volatile Tital Organics
Carbon
liO/l
*0.3 <0.4
*9.3 . <0.4
*9.9 *0.2
KP UP
*0.3 KF
KF NF
KF <0.2
KF <0.4
KF Hf
KF HP
KF HF
4 . `3
KF RF
<2 RF
KF RF
KP HP
KP . NF
KF HP
KF RF
KP HF
KP HP
KF HP
M
1.0
3.2
1.8
9.9 5.4
* 9,40 2.2
1.3 0.9
J.? 2.0
3.3 4.0
7.1 0.6
e.s
0.2
1.2 0.6
11.4
4.1
zt ^V-J
AP00009008
Table 11.7
Categories of Known or suspected Organic Chemical Carcinogens round in Drinking water
Compound Human Carcinogen*
Highest observed
concentrations in finished water fuc/1)___________
Upper 955 Confidence estimate of lifetime
cancer risk per uo/llter*_________
Vinyl Chloride** Suspected Human Carcinogens
10
5.1 X 10-*
Benzene Benxo(a) pyrene**
Animal Carcinogens
10 D.
X.D. X.D.
Dieldrin Kepcne
Heptachlor
Chlordane DDT/DDE Lindane (7-EHC)
c-BHC
fi-BbiC
PCS (Aroclor 126Qj
ETU_________________ / Chlororom
Caxoon tetracnlorrae PCNB Trichloroe thylen e Diphenylhydrazine Aldrin
-Suspected Animal Carcinogens
Bis (2-chloroethyl)ether Endrin Heptachlor epoxide
0
H.D.
D. 0.1
D.
0.01
D.
D.
3
_N.O.
j66 ~
N.D.
O.5
1 0.
0.42 0.08* D.
2.6-x 10-*
4.4 x 10-*
4.2 x 10-4
* 1.8 x 10-s
1.2 x 10-
J9.3 x 10-*
6.5 x 10--*
4.2 x 10--*
. 3.1 X 10-*
2.2 x 10-*
,' `jz
1 \j~t 1
T3 x 10-^
1.4 x 10-7
1.3 x 10-7
X.D.
X.D.
1.2 x 10--* X.D.
X.D.
I ' i.n
AP00009009
found the mortality rate for men aged 35-74 was 22/100#000 per year for smokers in a rural area vs. 50/100,000 per year for nonsmokers in an urban area. These numbers went up to 147/100,000 and 248/100,000 respectively for those smoking one pack of ciga rettes a day. The rural/l<iverpool difference could be attributed to the carcinogens produced by fossil fuel burning* In passing we note that they are somewhat synergistic with tobacco smoke. In the absence of complete information, it is conventional to take the concentration of benzo (a) pyrene as an indicator.
2 This is supported in part by a study of British gas workers. Pike3 in a recent review states "in the U.S. it would be prudent to equate 10 ng/m3 BP (benzo (cx) pyrene) pollution to one ciga
rette a day.'' In a typical city now, the BP concentrations are
I.5 ng/m leading to a risk of 2 x 10 ./year or 2000 cases of
lung cancer/year. Occupational levels are often 100 times higher, but with
more than 1000 times fewer people exposed. This gives a typical risk of 2 x 10*~3 occupationally, but only 200 cases a year.
In the enclosed Table II.6 is a list of air pollutant in air samples measured in various places.3^
-
II,15. Long term fate of carcinogens The long term fate of carcinogens is clearly of great concern.
Most of the organic carcinogens--even DDT and PCB's--break down in time, but the inorganic carcinogens--arsenic, chromate and so on--persist. These, however, are not primarily the fault of the
i
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Vapour
Table II.8
Vapour composition of the arbiem at-csphei*}* j
i.g/n
Samplin'] file
117
water
n-heptane
to1 vent
Isopentane Z-oethylhewnt n-p"ntanf *
2,3-direthylbutane
benzene w-hexanc
ethylbenzene 3-methylpentane 1 -1 thy1 3-nethy 1 benzene
ethylbenzene 1 *e thy1--me tHy1ben rene -octane 2-mctHylheptane
Isopropylbenzene
l-ethyl-2-nethvlbenzene 2-*ethy1-Z-butenr> fK::.*-buty1 benzene
. 1,2,4-trinethylbenzene propylbenzene n-nonane
wdodecane ZtW'i.-'-2-pentane
ft'Propylbenzene naphthalene r-deeanc n-undecene
1-penten*
2-methyl1-butene aylenes
2,2-direthylbutane eis-2-pentene
1,2,4,5* tetraethyl benzene 1,2,3,5-tetrarethylbeniene 1,1,1-trlentoroethane acrolein
acetaldehyde l*1,2-trichlorotrifIuoroethane
phenol piperazine earbaxoie penta^thylbenzene phenanthrene anthracene
tetrichloroethylene trichloroethylene methyl Iodide chloroform carbon tetrachloride p.p'-MT o,e'-D0T
chiordane PCB
10* 140
140
130 120 100
so
50 43 30
30 2B 25
IS 16
16 15
13
12 11
11 ID
9 9 9
8' 8 8 7
6 6 6 '4
4 4 4 1.5 X
X < 0.8-17
0.05 0.04
0.04 0.03 0.03
0.02
0.019
0.011
. 0.007
0.004 0.0004
0.00001-0.00003
0.00001-0.00004 < 0.009005-0.00009
0.0002-0.0004
Zurich
Los Angeles. Toronto
Los Angeles * Zurich Los Angeles
Los Angeles Los Angeles* Toronto Los Angeles Zurich Los Angeles Zurich Los Angeles Zyrich Zurich Zurich
Los Angeles Zurich Los Angeles Los Angeles Paris* Zurich Los Angeles Zurich Zurich Los Angeles Zurich
Los Angeles Paris Paris Los Angeles Los Angeles
Paris los Angeles Los Angeles Paris ^ Parts New Brunswick
6 US urban and non-grban areas St Louis* Ho. St Louis. Ho. St Louis, no. St Louis, Mo. Los Angeles - Los Angeles (background) (background) (background) (background) (background) Sargasso Sea Sargasso Sea Sargasso Sea Bermuda
* 8ean values; fee most of these pollutants* km values My be somewhat higher or lower In different parts of the world.
* t l :
f < t
VTZZ&
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118
chemical industry? arsenic enters the environment--15,000 tons per year of it-- as a pesticide sprayed upon crops.
It is In this matter of the long term fate of carcinogens that the Information is most uncertain. It is an area that, by its nature, needs national and even international attention, yet so far attention has been on the direct effects which are clearly small.
11.16. Summary
r
I summarize the calculations above of cancers per year
Occupational
Environmenta1
Asbestos
120
less than 12
Arsenic
200/yr
Vinyl Chloride
less than 1/yr
less than 1/yr
Polycyclic hydrocarbons benzo (cM pyrene as indicator
200/year
2000/year
Water (chloroform, aflatoxin, dieldrin)
20/year
Benzene
less than 1/yr
less than 1/yr
Worst case estimates
Bladder cancers
2,200/year
?
Liver cancers
350/year
?
Kidney cancers .Lung cancers
2,000/year 1,000/year
? ?
Total
5,500/year
This total of occupational cancers is 1-3% of all cancers in
i
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*
i
119
agreement with the distinguished authorities mentioned. This is a number worth reducing but it is not large compared with all the other occupational hazards--accidents and so forth.
i
i
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REFERENCES
120
1. S.S. Epstein in "Environmental Determinants of Cancer," Cancer Res., 34 2425 (1974), without going through the number for any chemicaT, seems to believe this argument.
2. J.S. Higginson, M.D. and C.S. Muir, M.D., "The role of epidemiology in elucidating the role of environmental effects in human cancer," Cancer Res, and Prev., :L 1, 79 (1976).
3. . Sir Richard Doll, "Strategy for detection of cancer hazards in man," Nature, 265 569 (1977).
4. E.L. Wynder, "Nutrition and Cancer," Proceedings of the Federa tion of the American Societies for Experimental Biology, 35 1309 (1976).
5. G.B. Gori and E.l. Wynder (Editorial) "Contribution of the Environment to Cancer Incidence--An. Epidemiological Exercise,"
. Journ. Nat. Cane. Instit., 58 25 (1977).
6. J. Higginson, "Present Trends in Cancer Epidemiology," Canad. Cancer Conf. 3 (1969) Pergamon.
7. J. Higginson, "Cancer Etiology and Prevention," in Persons at
High Risk of Cancer; An Approach to Cancer Etiology and Control,
ed.J. Fraumeni (1975).
8.' J. Higginson, "Population studies on cancer action," Un. Inst. Cancer 16 1667 (1960).
9. M. Segi and M. Kurihara, Cancer Mortalley in 24 Countries/ Nagoya, Japan Cancer Society No. 6~(1972).
10. R. Doll, C. Muir, and J. Waterhouse, eds.. Cancer Incidence in . Five Continents, A technical report, vols. I and II. Springer Verlay, Berlin and N.Y. (1570}*
11.
T.J. Mason, F.w. McKay, R. Hoover, W.J. Blot and J.F. Fraumeni,
Atlas of Cancer Mortalities for U.S. Counties 1950-1969, U.S.
Dept, of Health, Education, and Welfare, National Institutes
of Health NIH-75-780 (1975).
,*
12. Sir Richard Doll,"Strategy for detection of cancer hazards to man," Nature, 265 569 (1977).
13.
Chloroform is caused by chlorination of drinking water as the chlorine interacts with organic matter. It Is not a strictly
natural cause, but it's not the fault of the chemical industry.
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12 L
14. W.J. Blot and J.F. Freumeni, Lancet, July 26, 1975, page 142 and private communication with W.F. Blot.
15. Testimony of Richard Wilson to OSHA Hearing on the Emergency Standard for Occupational Exposure to Ben2ene.
16. I.R. Tabershaw and V7.R. Gaffey, "Mortality Studies of Workers in the Manufacture of Vinyl Chloride and Its Polymers#" 3. Occup. Hed., 16# 509 (1974).
17.
Monson, R.R., J.M. Peters, M.lN. Johnson# "Proportional Mortal
ity Among Vinyl Chloride Workers#" Ann. N.Y. Acad. of-Scl., 246, 225 (1975).
18.
I.J. Selikoff and E.w. Hammond# "Environmental Cancer#" in Persons at High Risk of Cancer, An Approach to Etiology and Control, ed. by~J~.F.~ Fraumeni, Academic Press (1975). .
19.
* /\
.20
./? 21
22.
I.J. Selikoff, W.J. Nicholson and A.M. Langer, Arch. Env. Health, 25 1 (1972).
F*.A. Lundin, W. Floyd, E.M. Smith, V.E. Archer and D.A. Haladay# Health Physics, 16, 371 (1969).
R. Hoover and J.F. Fraumeni, Cancer Mortality in U.S. Countieswith Chemical Industries# Env..Res.# 9 196 (1975)
I note that in the most extreme county*, where the rate of blad der cancer among white males is 16/100/year, the total number of cases in 19 years is still only 73.
23.
H.B. Demopoulous, "A Rational View of Cancer in New. Jersey," Report available from N.J. State Chamber of Commerce# 5 Commerce Street, Newark, NJ 07102.
24. R.A.M. Case, M.E. Hasker, D.B. McDonald, Brit. Joum. In. Med., (1954).
25.
"Drinking Water and Health#" report of the Committee on Safe Drinking Water# Advisory Committee on Toxicology# National Academy of Sciences/National Research Council# May 1977.
26. National Organics Reconnaissance Survey# Water Quality Data,
U.S. Environmental Protection Agency.
%
27. "Air Pollution and Human Health," L. Lave and E. Seskin, Science# 169# 723 (1970).
28. P. Stocks, supplement to British Empire Cancer Campaign Annual Report (1957).
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% 122
29. P.J. Lawther, B.T. Commins, R.E. Waller, Brit. J. In. Med.. 22, 13 (1965).
30.
Malcolm C. Pike, R.J. Gordon, B.E. Henderson, H.R. Menck,
Jennie Soottoo, "Air Pollution," in Persons at High Risk of Cancer, ed. *J.F. Fraumeni, Academic Press, New York (1975)
31.
E. Sawicki, "Chemical composition and potential genotoxic aspects of polluted atmosphere," in Air Pollution and Cancer In Man, ed. U. Mohr, D. Schmahl, and L. Tomatis, IARC Scien tific Publications Mo. 16, WHO, Lyon, France, 1977, p. 134.
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