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Asbestos Exposure,
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Smoking, ancl Neoplasia
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In'ing /. ScliholJ. Ml): E. Cuyler Hammond. Scl); and Jacob C.hmg, Ml)
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Asbestos insulation workers, as a group, have a high risk of dying of bronchogenic carcinoma (about seven or eight times expected). We have observed 370 such work men from Jan 1, 1963 to April 30, 1967. Our findings indicate that asbestos exposure alone is not the entire explanation. Of 87 noncigarette smokers, none died of bronchogenic carcinoma. Of 283 workmen with a history of regular cigarette smoking, 24 died of bronchogenic carcinoma, although only three were expected to die of this disease. Calculations suggest that asbestos workers who smoke have about 92 times the risk of dying of bronchogenic carcinoma as men who neither work with asbestos nor smoke cigarettes. We conclude that asbestos exposure should be minimized, that asbestos workers who do not smoke should never start, and that those now smoking should stop immediately.
n 1964, we reported on deaths occurring between Jan 1, 1943. and Dec 31. 1962, among 632
due to chance, the number of such deaths being small. During the latter part of the study, we ob tained information on the smoking habits of most of the survivors, but we could not obtain reliable information on the smoking habits of those who had died at an earlier date. Therefore, we could not at that time investigate death rates in rela tion to smoking habits and exposure to asbestos dust which were considered both separately and jointly.
There is abundant evidence that.cigarette smok ing leads to a high rate of death from lung cancer in the absence of occupational exposure to asbestos dust." 1 Our findings outlined above suggested (but did not prove) that exposure to asbestos dust may lead to a high rate of death from lung cancer in the absence of cigarette smoking. If the latter be so, then the combined effect of both types of ex- , posure might or might not he equal to or greater
the enl she tio: anc firs dal bee the die' anc 30,
I me; eve upc incl arni hab
members of the International Association of Heat than the sum of the two effects. On the other hand,
cur
and Frost Insulators and Asbestos Workers.1 All of these men had been occupationally exposed to
it was possible that exposure to asbestos dust in- . creases the risk of lung cancer among cigarette
exa and
asbestos dust for many years. Their death rate from lung cancer was found to be 6.8 times as high
smokers but does not lead to lung cancer among,
nonsmokers.
' ''
are I.
as that reported for the genera! white male popu
The present study was undertaken primarily
pen
lation of the United States during the same years, to investigate these possibilities.. In addition, >e
ami
.with, age taken, into- consideration. Three of the wished to obtain more' information on the occur
six
men died of diffuse pleural mesothelioma and one rence of mesothelioma and gastrointestinal cancer
five
died of a neoplasm histologically suggestive of peri among asbestos workers.
, unic
toneal mesothelioma. This was of interest since mesothelioma is a very rare disease in the general
Material
. well and
population but is reported to be associated with
From records of New York Local 12 and Newark, . the
exposure to asbestos dust.' In addition, their death NJ, Local 32 of the International Association of ' the
rate from cancer of the stomach, colon, and rectum Heat and Frost Insulators and Asbestos Workers, ` on c
was higher than expected: but this may have been
From (he Department of Comtminifv Mcdirinc. Mount Sinai School of Medicine (Drs. SelikofT nnd Chun?), nnd the Depart
a list was made of every man who was a member of either one of these locals on Dec 31, 1942, or who joined between that date and Dec 31, 1962.
by chai
196'
ment of Kpidemiolouv nnd Statistics. American Cancer Society (Dr. Hammond), New York.
Read before a joint meeting of the Section on Diseases of the Chest with the Section on Preventive Medicine and the American
No one was omitted regardless of his subsequent
work history.
`
Personnel data from union records indicated that
0 smo smo
College of Chest Physicians at the IK5th annual convention of the
American Medical Association, Atlantic City, NJ, June L9, 1967-
Reprint requests to Mount Sinai School of Medicine. 100th
Street and Fifth Avenue. New York 10029 (Dr. Selikoff).
-
of the 632 on the union rolls on Jan 1, 1943, 339 of the men had first been occupationally exposed .
dust prior to 1922, and an additional :
ciga ciga the
104 JAMA. April 8. 1968 Vol 204, No 2 ' JAM/
being we obf most eliable e who
could ei rela-bestos iv and
smokcancer sbestos d (but st may ncer in iter be of exireater .hand, ust iniarette among
imarily on, we occurcancer
.'ewark, tion .of 'orkers, n ember 942, or , 1962. sequent
ed that 43, 339 exposed ditional
-04. No 2
ASBESTOS EXPOSURE-SELIKOFF ET AL
107
293 men had first been ex posed between the be
Table 1.--Subjects Classified by Age as of Jan 1, 1963. and by Years From First Occupational Exposure to Asbestos Dust up to Jan 1, 1963
ginning of 1923 and the end of 1942. All of these men were successfully traced through Dec 31, 1962, and 262 of them were found to have died up to that time. Of the 262 deaths, seven oc curred prior to the 20th anniversary of the man's first exposure to asbestos
Age, Yr
35-39 40*44 45-49 50*54 55-59 60*64 65-69 70*74 75-79 80*84
Total
Total No. of Subjects
2 13 32 109 60 42 49 38 21
4
' 20-24 2
22 17
370 31
No. of Years Since First Exposure to Asbestos
25-29
30*34
35*39
40-44
45-49
50+
1 ...
2
13 a
... ... '
1 80 28
1 16 34 8 1
1
3 11
19
8
1 10 18 18
2
...
3 12
6 17
... . .
1 5 15
... ...
1i2
6 113 86 59 39 36
No. of
52 Mo
1 2 18 11 16 17 18 8 3
94
dust and 255 occurred
after the 20th anniver sary. Thus, of the 632 men, 370 were still living on Jan 1, 1963.
These 370 men were the subjects of the pres ent investigation. Table 1 shows their age distribu tion as of Jan 1, 1963, and the lapsed time from first exposure up to that date. All of them have been traced, and 94 of
Table 2.--Subjects Classified by Age and by Smoking Habits on or about Jan 1, 1963
Age, Yr
35-39 40-44 45-49 50-54 55-59 60-64
65-69 70-74
75-79 80-84
Total No. 2 13 32
109 60
42 49 38 21
4
Smoked Regularly
1 2 2 12 6 7 6 7 3 2
Pipe, Cigar Only
1 6 5 4 8 7 7 1
Ex* cigarette Smokers*4
1 2 5 26 16 15 17 12 6 1
Current Cigarette Smokers*
1*9 a Oay'
...
. 3..
1
,.1. ...
10-19 a Oay
5 3
4 4 1
20*39
a..D.ay
5 12 33 20 11 9 4
3
40+ '
a..O.ay
4
12 24
10 4
5 3
1
Total
370
48
39 101
5 17 97 63
them were found to have
* includes cigarette smokers who also smoked pipes or cigars.
died during the four-year
and four-month interval from Jan 1, 1963, to April 101 were excigarette smokers, five currently smoked
30, 1967.
one to nine cigarettes a day, 17 smoked 10 to 19
Beginning in October 1962, we made arrange cigarettes a day, 97 smoked 20 to 39 cigarettes a
ments to examine these men periodically, once day, and 63 smoked 40 or more cigarettes a day.
every six to twelve months; the interval depended
The smoking habits of the 370 subjects were
upon age and physical condition. The examinations compared with the-smoking habits of a large num
include chest x-ray films as well as physical ex ber of men selected from the general population.'1
amination and cover past and present smoking There were proportionally more cigarette smokers
habits, occupational history, medical history, and among the 370 subjects than were found in the
current physical complaints. Altogether, w'e have general population sample; age was taken into
.examined 338 (91.4) of the men at least once consideration.
and have repeatedly examined most of those who
Causes of Death.--A copy of the death certificate
are still living.
was obtained for each of the 94 deaths. In addi
Information on smoking habits was obtained by tion, we examined hospital records, postmortem
personal interview with the 338 men who were ex findings (41 cases), as well as the surgical and
amined. Of the 32 men who were not examined, pathologic reports when surgery was performed (39
six told us their smoking habits by telephone and cases). We also reexamined histologic specimens.
five gave us the information by mail. The local It was found that the death certificate was inac
union secretaries (who personally knew these men curate in 14 instances.. However,- this-did-not-alter
. well) ascertained-the- smoking habits of 18 men, the picture as much as might have been expected
and family members supplied the information on since there were several compensating errors. For
the remaining three men. This accounts for all of example, in one instance the death certificate in
the 370 men. Table 2 shows their smoking habits dicated bronchogenic carcinoma as the cause of
on or about Jan 1, 1963, the men being classified death while a review of the histologic specimen
by their ages on that date, even though some showed that death was due to pleural mesothe
changed their smoking habits between 1963 and 1967.
lioma; but in another instance exactly the reverse was found. Likewise, review in one instance re
Of the 370 men, 48 never smoked regularly, 39 sulted in changing the reported cause of death
smoked or had smoked pipes or cigars but never from bronchogenic carcinoma to cancer of the
smoked cigarettes regularly, and 283 had smoked stomach with metastasis to the lungs while review
cigarettes regularly. Some of those with history of in another instance resulted in exactly the oposite
cigarette smoking also smoked pipes or cigars. Of change. The 94 deaths were ascribed to the follow
the 283 with a history of regular cigarette smoking, ing causes: bronchogenic carcinoma, 24; pleural
JAMA, April 8, 1968 Vol 204, No 2
SO(M0?42
105
iWS&fc-'V"'-* '5 i4ii&4i*U*ZiA
I'<h! mitdOMiM
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108 ASBESTOS EXP0SURE-SEL1K0FF ET AL
Table 3.--Observed end Expected Number of Deaths Among 370 Asbestos Workers During the 52-Month Period
Cause of Oeath T.otal, cancer (all stes>
Cancer of lung, pleura, bronchus, and trachea Bronchogenic carcinoma Pleural mesothelioma
Peritoneal mesothelioma Cancer of stomach ` Cancer of colon and rectum Cancer of all other sites combined Asbestosis Heart and circulatory disease including stroke AH other causes of death
Total, all causes
Observed Deaths 49
27 24
3 7 3 5 7 15
22 8
94
Expected Deaths*
8.6
2.3 r i i 0.6 1.2 4.5
. ..
23.5 10.4
47.5
8ased upon US mortality data disregarding smoking habits.
iUmted States data not available, but figure should be only slightly less than 2.3.
tUmted States data not available, but these are rare causes of death
in general population.
mesothelioma, three; peritoneal mesothelioma, sev en: cancer of the colon, four; cancer of the rectum, one: cancer of the stomach, three: cancer of the pancreas, two: cancer of buccal cavity and pharynx, two: cancer of bladder, one; cancer of undeter mined primary site, two; asbestosis, 15; cor pul monale. one; cornary heart disease, 17; congestive heart failure, one; cerebral vascular lesion, two; aortic aneurysm, one; cirrhosis of the liver, three; bronchopneumonia, one; encephalopathy, one; acute pancreatitis, one: Wegener's granulomatosis, one: and accidental fall. one.
Expected Deaths.--For purposes of comparison, we wished to ascertain how many of the 370 sub jects would have died during the 52-month period (Jan 1. 1963, to April 30, 1967) if their age-specific death rates had been exactly the same as for the general white male population of the United States. For this purpose, we made use of the United States 1964 life table for white males; this provided the most stable basis for comparison. It should be noted that for white males total death rates and death rates from respiratory cancer were slightly higher in the industrial states of New York and New Jersey than in the United States as a whole."r On the other hand, respiratory cancer death rates in white men aged 20 to 64 are reported to be a trifle .lower than average among laborers, not elsewhere classified employed in construction work.'1
From the life table we determined for each of the 370 men the probability of his dying within a pe riod of 52 months, considering his age on Jan 1, 1963. and assuming that the life table probability applied to him. Summing these probabilities for the 370 men yielded an estimate of the "expected" number of deaths under the null hypothesis that the age-specific death rates of these asbestos work ers are the same as for United States white males in general. The computation indicated that 47.5 deaths would have been expected.
Next, we wished to estimate the expected num ber of deaths from each of several causes. For this, we made use of the percentage distribution of deaths by cause of death among United States
106
white males of various ages during the year 1964
as reported by the National Center for Health Sta-
tistics. These percentages were then standardized
for age according to' the age distribution at time
of the 47.5 expected deaths. The results are shown
in Table 3.
:
Expected vs Observed Deaths.--As shown in
Table 3, there were 94 observed deaths (ie, 94 of
the 370 asbestos workers died) as compared with '
47.5 deaths expected on the basis of the age-specific
death rates of all white males in the United States
in 1964. Thus, there were 94 minus 47.5 = 46.5
excess deaths. The excess deaths were due to bron
chogenic carcinoma, mesothelioma of the pleura
and peritoneum, asbestosis, and cancer of the
stomach, colon, and rectum.
Cancer of Lung, Pleura, and Trachea.--In pub- '
lished mortality data for the United States show
ing deaths each year from various causes by age,
sex, and race, the following diseases are combined:
cancer of the lung (including sarcoma of the lung),
cancer of the bronchus, cancer of the pleura, and
cancer of the trachea. For this group of diseases,
there were 27 observed deaths and only 2.3 ex-
pected deaths, a ratio of nearly 12 to 1.
It is well known that, for the United States as
a whole, all except a very few of the deaths re
ported in the combined category are due to bron
chogenic carcinoma. Thus, it may be assumed that
there were ciose to 2.3 expected deaths from this
cause as compared with 24 observed deaths, a ratio
of over 10 to I.
.
Mesothelioma.--Ten of the 94 observed deaths
were due to mesothelioma, three were due to
pleural mesothelioma, and seven were due to peri
toneal mesotheliomas. This is such a rare disease
mat if the 370 subjects had been selected as a
random sample from the general population, one
would not have expected any of them to die of
mesothelioma within a period of 52 months.
All three of the men who died of pleural meso
thelioma had a history of regular cigarette smoking.^
Of the seven who died of peritoneal mesothelioma,
one never smoked regularly, one smoked only pipes '
and cigars, and five had a history of regular ciga
rette smoking-.
'
Cancer of Stomach, Colon, and Rectum.--In our
earlier study of asbestos workers,1 there were more
deaths than expected from cancer of the stomach,
colon, and rectum (9.4 expected, 29 observed). As i
compared with a total of 1.8 expected deaths from
these causes, there were eight observed deaths in
this study, due to cancer of the following sites: '
stomach, three; colon, four; and rectum, one. Al
though this bears out our earlier findings, the num-
her of deaths from these causes was so small that ;
we still refrain from drawing any conclusion at
this time.
'
jf
Asbestosis.--Asbestosis accounted for 15 of the >
94 deaths. While it is not surprising that deaths
from this disease occur among men exposed to ]
kasbestos dust, attention must be called to the fact >
5O010243
JAMA, April 8. 1968 Vol 204, No 2 I
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ASBESTOS EXPOSURE-SELIKOFF ET AL
' 109
that these subjects were primarily insulation work
Table 4.--Estimated Number of Lung Cancer Deaths Expected to Occur During a Period of 52 Months per 10,000 Men Living at the Start of Period: by Age and by Smoking Habits*
ers. While all of them were occupationally ex posed to asbestos dust, their degree of exposure was light as compared with the degree of ex posure of asbestos miners, processors, and weavers in earlier times.
Bronchogenic Carcinoma.-Bronchogenic car cinoma accounted for 24 deaths while only about 2.3 were expected on the
Act. Yr {Jan 1, 1963)
35-39 40-44
45*49 50-54 55-59 60-64
65-69 70-74
75-79 80-84
Never Smoked Regularly
0 2 z 7
6 16 14
12 28
25
Pipe, Cigar Only
...r . -
2 12 15 31 32 52 53 32
Excigarette Smokers?
5
7 10 22 S3 71 97 100 100 148
1-9 a Day
...
., . .
,.
.28
,. 80
103
Current Cigarette Smokers?
10-19 a Day
.a .
,. . ,.
44 91
157 206 185
20-39 a Day
15 39 69 117 190 305 288 341
40-4-
a .D.a.y
15 46 90 185 256 350* 450* 329
`
Based upon data from a prospective study with adjustment for US mortality experience. {Ellipses indicate rates omitted for categories with no subjects in this study. See Table 2. tlncludes cigarette smokers who also smoked pipe or cigar. Men with a history of only cigarette
smoking have higher lung cancer rates than snown here. Rates obtained by smoothing the data.
basis of general United States mortality data for divided into many five-year age groups, some of the
white males. However, as previously mentioned, subgroups contained only a small number of men.
evidence at hand suggests that there were propor In consequence, the lung cancer death rate was
tionally somewhat more cigarette smokers among statistically unstable in some of the very small sub
the 370 subjects than among white males in the groups. In three instances where the observed rate
United States as a whole, age being taken into in a small subgroup appeared to be badly out of
consideration. This might have partially accounted line, we arbitrarily made an adjustment to bring it
for the high bronchogenic carcinoma death rate of more into line with adjacent figures in the table.
the subjects. For this and other reasons we made These adjusted figures which are indicated with
estimates of the expected number of bronchogenic symbols in Table 4 carry very little weight in the
carcinoma deaths, the smoking habits of the men final calculation. All of the rates were then ad
being taken into consideration. This was done as justed as follows:
follows:
Lung cancer death rates in the United States
Data are available on lung cancer deaths in re have risen steadily year by year and were higher
lation to the smoking habits of 440,000 men en in 1964 than during the period 1960 to 1964 as a
rolled by American Cancer Society volunteers in whole. Furthermore, in the study described above,
a prospective epidemiological study between Oc we avoided enrolling seriously ill people and, as of
tober 1959 and March 1960 and "traced through the cut-off date for preparing the computer tape,
Sept 30,1964. Causes of death were ascertained from we had not yet received death certificates for all
death certificates, but whenever cancer was men of the men now known' to have died during the
tioned on a death certificate inquiry was made of specified period of time. For these reasons, lung
the physician who signed the certificate. In case cancer death rates in the study population were
of disagreement between the two sources of infor appreciably lower than those reported for white
mation. the physician's statement was accepted. males in the United States in 1964. To compensate
For the purpose at hand, we only made use of data for this, we raised the rate of each individual smok-%
covering the 52-month period beginning on June 1. ing category so that the total lung cancer dea'th'
1960. and ending on Sept 30. 1964. The number of rate (disregarding smoking habits) in each five-
lung cancer deaths occurring during the 52-month year age group would be the same as that of all
period was divided by the number of men alive at United States-white males"!basetl upon the 1964
the beginning of the period. This was done by five- life table and the 1964 distribution of deaths by
year age groups for men in each of the following causes of death). The results of these computations
smoking categories: (1) never smoked regularly are shown in Table 4. (It should be noted that
(nonsmokers and occasional smokers being com Table 4 shows only such rates as were required for
bined); (2) history of regular pipe or cigar smok further calculations.)
ing. past or present, but never smoked cigarettes
The rates shown in Table 4 were then applied to
regularly; (3) excigarette smokers (including those the number of asbestos workers shown in each of
who had smoked or currently smoked pipes or the corresponding internal cells of Table 2. This
cigars); and (4) current regular cigarette smokers yielded an estimate of the number of lung cancer
(including those who also had smoked or currently deaths expected to occur during a 52-month period
smoked pipes or cigars). The last of these cate among the 370 asbestos workers classified by their
gories was further divided by current number of smoking habits. By "expected" number, we here
cigarettes smoked per day: (4a) one to nine ciga mean an estimate of the number of lung cancer
rettes a day; (4b) 10 to 19 cigarettes a day; (4c) deaths which would have occurred under the null
20 to 39 cigarettes a day; and (4d) 40 or more hypothesis that asbestos workers do not differ from
cigarettes a day. Since the men were divided into other men in respect to their lung cancer death
seven groups by smoking habits and further sub
smoking habits being taken
JAMA, April 8. 1968 Vol 204, No 2
irfc
HQ ASBESTOS EXPOSURE--SELIKOFF ET AL
Table 5.--Observed and Expected Bronchogenic Carcinoma Deaths by Smoking Habits* for 370 Asbestos Workers
Smoking Habits Never smoked regularly History of pipe, cigar smoking only History of regular cigarette smokingt
Total
Observed Deaths 0 0 24
24
Expected Deaths 0.05 0.13 2.98
3,16
''Based upon data in Table 2 and Table 4. t Includes cigarette smokers who also smoked pipe or cigar,.
Table 6.--Expected and Observed Deaths Among 632 Asbes tos Workers Exposed to Asbesto Dust 20 years or Longer
Total deaths: all causes Exoccted
Observed
Total cancer: all sites Expected
Observed
Cancer of lung, trachea, pleura Expected
Observed
Cancer of stomach, colon, rectum Expected
Observed
Cancer all other sites combined
Expected
,
Observed
Asbestosis Exoected
Observed
All other causes Expected
Observed
1943-1962
203.5 255
Total 1963-1967 1943-1967
47.5 94
251 349
36.5 95
6.6 49
45.1 144
6.6 45
2.3 27
8.9 72
9.4 29
1.8 11.2 8 37
20.5 21
4.5 14
25 35
00
0
12 15 27
167
38.9
205.9
148 30 178
into consideration. The results are summarized in Table 5 which shows the expected and observed number of lung cancer deaths in each of three smoking categories.
Taking smoking habits as well as age into con sideration (Table 5) a total of 3.2 bronchogenic carcinoma deaths were expected whereas taking only age into consideration 2.3 deaths were ex pected from this cause (Table 3). Thus, perhaps one of the excess bronchogenic carcinoma deaths might be attributed to the fact that there appear to have been proportionally somewhat more ciga rette smokers among the 370 subjects than among men of the same ages in the general population.
The following statements are based upon the data shown in Table 5. Twenty-four deaths from bronchogenic carcinoma occurred among the 370 subjects compared with only 3.16 expected, a ratio of about 7.6 to 1. This is slightly higher than found in our earlier study which indicated a ratio of 6.8 to 1 (not taking smoking habits into considera tion). It should be noted in this connection that the 370 subjects in this study had been exposed to asbestos dust somewhat longer than the subjects of our previous study (the present 370 subjects are survivors as of Jan 1, 1963, of subjects in the previous study).
Of the subjects who never smoked regularly and those who smoked only pipes or cigars, none died of bronchogenic carcinoma whereas 0.18 of these men were expected to die of lung cancer. This sug gests that exposure to asbestos dust does not in crease the risk of bronchogenic carcinoma among
men who never smoked cigarettes regularly. How
ever, considering the small number of such subjects
in this study, we only conclude that exposure to
asbestos dust does not greatly increase the risk of
bronchogenic carcinoma among men who never
smoked cigarettes regularly.
Twenty-four of the men with a history of regular
cigarette smoking died of bronchogenic carcinoma
whereas only 2.98 were expected to die of it, a ratio
of 8.05 to 1. From this it appears that exposure to
asbestos dust greatly increases the risk of lung
cancer among cigarette smokers.
Now we may ask how greatly is the risk of bron
chogenic carcinoma increased by the combined ef
fects of cigarette smoking and exposure to asbestos
dust. To answer this question, we applied rates
shown in Table 4 for nonasbestos workers who
never smoked regularly to the number of subjects
with a history of regular cigarette smoking as shown
in Table 2. This indicated that only 0.26 of the
subjects with a history of regular cigarette smoking
would have been expected to die of bronchogenic
carcinoma if they had never smoked regularly and
had never been occupationally exposed to asbestos
dust. Since 24 of them actually died of this cause.
the ratio of observed to expected deaths is 92 to 1
(ie, 24 divided by 0.26=92). This appears to in
dicate that cigarette smoking plus occupational
exposure to asbestos dust increases the risk o;
bronchogenic carcinoma by a factor in the order oi
magnitude of 92 to 1. It should be noted that this
estimate does not take current amount of cigarette
smoking into consideration.
Comparison With Earlier Findings.--As explained.
we started with a cohort of 632 asbestos insulation
workers, the entire membership, of the union locals
on Jan 1, 1943. We have now traced each man
through April 30, 1967. Table 6 shows the observed
and expected number of deaths for each of two
periods (the first. 1943 to 1962, being previously
reported') and for the entire period. In respect to
respiratory cancer (lung, trachea, and pleuraX and
in respect to cancer of the stomach, coldn,' and
rectum, the findings in the two periods are in close
agreement.
.
i 1 < t
1 ' T f f ' )' t" 115 r" 0
r` C;
Comment
The increased risk of neoplasia (mainly broncho genic carcinoma and mesothelioma) among insula tion workers reported here should be evaluated in b the knowledge that these men have comparatively nf light exposure as asbestos trades go. Primarily em-*' ployed in construction work, many of the materials >' they use contain little or no asbestos and other; to have only 5% to 15%. Conditions of work vary; these men often work outdoors unlike asbestos sfoperators in factory work. Comparatively few dust- l,( exposure surveys have been made in this trade but a-" their results have generally been within the 5 mil- 1 lion particles per cubic foot permissible limits cur- oc rently accepted by the American Conference ol Governmental Industrial Hygienists.0-10 Nor have nt
509^0745
108 JAMA, April 8. 1968 Vol 204. No! JA
ASBESTOS EXPOSURE-SELIKOFF ET AL
in
wjts ; to of \ jet f
.lar 1 ma 1 tio to mg
onefitS ites .vho jets
jwn the
:ing enic
and sios
use, to 1 i in.onal k of er of this rette
`f ; /
.
ined, ation ocals man erved
two
ously :Ct to ) and .. and . close
)neho-:Insula ted inatively :iy emiterials others : vary; sbestos w dustade but ; 5 milits curence of or have
204. No 2
additional potentially carcinogenic substances been identified among the other materials used.10
Heavier or even lighter exposure may result in different degrees of risk of neoplasia. Heavy factory exposure in the past has in some instances resulted in considerable lung cancer risk." In others, para doxically, little lung cancer was seen because asbestosis was so common and so severe as to cause death of the exposed workers before they could live long enough to develop lung cancer. Once exposure was reduced by improved industrial hygiene prac tices, early death from asbestosis sharply dimin ished and lung cancer became common.1'
In any case, heavy exposure is not likely to be the most important problem in the future, unless there be sheer carelessness or unconcern. Rather, light exposure, similar to that in insulation work, will be much more common, both in direct asbestos working trades and as the result of indirect occupa tional exposure, as in the construction and ship building industries.
There is another type of "light exposure" which may affect many more people than those industrial ly exposed. In the past several years, it has been demonstrated that asbestos bodies can be found in the lungs of 25% to 50% of adults examined at autopsy in large cities, such as Belfast, Northern Ireland, Capetown, Republic of South Africa, .Miami, Fla, Pittsburgh, and Montreal. This is presumably due to "asbestos air pollution" by libers derived from industrial "spillover" (as dust from construction sites or factory wastes) or from end-product use. ' Such community asbestos air pollution may be important since there is already evidence that in certain circumstances, as living within half mile of an asbestos plant or in the household of an asbestos worker, intimate environ mental contamination can be associated with some risk of mesothelioma.1'1 What is not now known is whether the minimal amounts inhaled by the geneinl public carry a similar risk.1'1
Nor do we know whether inhalation of the very ' small amounts of asbestos present in the air of some communities is associated with a special lung cancer risk in cigarette smokers (or. conversely, whether cigarette smoking makes the inhalation of very small amounts of asbestos particularly hazard . oust. It will be important to ascertain whether such'" cocarcinogonic or potentiating or precipitating rela tionships exist because, with the rapid growth of asbestos use (500,000 tons per year world produc tion in 1930 has risen to over 4,000.000 tons per year now), it may be difficult for cigarette smokers to avoid inhaling air contaminated with asbestos.
It may not be easy to unravel the interrelation ships which might exist between community as bestos air pollution and cigarette smoking. Both asbestos exposure and cigarette smoking have a long-lapsed period between onset of exposure and occurrence of neoplasia, yet for current smokers these two exposures may not have begun simulta neously; there was much less asbestos used 20 to
JAMA, April 8,1968 Vol 204. No 2
40 years ago. Youngsters who start smoking now have a much greater chance of having both ex posures simultaneously.
Significance of Findings for Asbestos Workers.-- The import of the data reported here seems clear. There is an extraordinary risk of developing and dying from lung cancer for asbestos workers who smoke cigarettes regularly. In the group studied, the combination of asbestos exposure and cigarette smoking increased the risk approximately 90 times compared with men who neither work with asbestos nor smoke!
Of 283 asbestos workers who had a history of cigarette smoking, 78 died within a period of 52 months whereas only 32.4 would have been ex pected to die within that length of time if their age specific death rates had been the same as for the general white male population of the United States. Of the 78 deaths. 24 (31%) were due to broncho genic carcinoma. It is estimated that if these men had smoked cigarettes but had not been exposed to asbestos dust, only 2.98 would have died of bron chogenic carcinoma within the same length of time. If they had neither smoked nor been exposed to asbestos dust, only 0.26 would have been expected to die of the disease within a period of 52 months.
Of 87 asbestos workers who never smoked ciga rettes regularly, none died of lung cancer within the 52-month period (although three died of asbestosis and one died of peritoneal mesothelioma). This finding, being based upon the experience of only 87 men. does not prove that exposure to asbestos dust has no influence on the risk of lung cancer among nonsmokers. However, it suggests that ex posure to asbestos dust does not lead to an ex tremely high risk of lung cancer among nonsmokers.
The conclusions are evident: 1. Occupational exposure to asbestos dust should be reduced to as low a level as possible; but there may be an irreducible minimum level if asbestos, a very useful material, is to be used at all. Such reduction in exposure will benefit asbestos workers of the future. However, we are also concerned with workers who have already been exposed at signifi cant levels for many years. Asbestos fibers Will rifemain in their tissues for the remainder of their lives. 2. All people incur a great increase in risk of lung cancer if. they smoke cigarettes; for asbestos work ers the increase in risk is tremendous. Asbestos workers who do not now smoke cigarettes should never begin. Those who do smoke, should stop immediately. We may hope that the decrease in risk which results from cessation of smoking among the general public1 will be the good fortune of the asbestos workers as well.
This investination was supported by the Health Research Coun cil of the City of New York.
References
X. Selikoff. I.J.; Churg. J.; and Hammond, E.C.: Asbestos Ex posure and Neoplasia. JAMA 188:22-26 (April (>) 19(54.
2. Selikoff, I.J.; Churg. J.; and Hammond, E.C.: Relation Be tween Exposure to Asbestos and Mesothelioma, New Eng J Med 272:560-565 (March 18) 1965.
50010246
109
11 "Vt.r A1
'>Ul^ 1J1'41111 .. .
iU xxiSmiitiiilSiti, irt\.
112 ASBESTOS EXPOSURE--SELIKOFF ET AL
3. Hammond. E.C.: "Smoking in Relation to the Death Rates of 3.000.000 Men and Women," in Kpideminlngical Study of Cancer and Other Chronic Diseases. Bethesda. Md: National Cancer Institute. 196fi, monograph 19. pp 127-204.
4. Smoking and Health. Report of the Advisory Committee to the Surgeon General of the Public Health Service, publication 1103. US Dept of Health, Education, and Welfare. 19154.
5. Hammond, E.C.. and Garfinkel, L.: Changes in Cigarette Smoking 1959-1905, Amer 1 Public Health 58:30-45 Man) 1968.
6. Vital Statistics oi the United Slates. 1900, part A. US Dept of Health. Education, anti Welfare. 1963. vol 2.
7. Death Rates From Malignant Neoplasms. I960. Public Health Service, publication 1113, US Dept of Health, Education, and Welfare. 1963.
8. Mortality by Occupation and Cause of Death, Public Health Service. US Dept of Health, Education, and Welfare, Vital Sta
tistics Division, Vital Statistics-Special Reports, 53:323 (Sept)
1963.
i
9. Fleischer, W.E.. et nl: A Health Survey of Pipe-Covering j
Operations in Constructing Naval Vessels, J Industr Hyg Toxic i.
28:9-16 (.fant 1946.
*
10. Keane. W.T., and Zavon. M.R.: Occupational Hazards of i ,
Pipe Insulators. Arch Environ Health 13:171-178 (Aug) 1966. <
11. Doll. R.: Mortality From I.ung Cancer in Asbestos Workers, I
Brit J Industr Med 12:81-86 (April) 1955.
1.
12. Jacob. G,, and Anspach. M.: Pulmonary Neoplasia Among ! ,
Dresden Asbestos Workers, Ann NY Acad Sc 132:536-548 (Dec
31) 1965.
f ' "
13. Newhouse. MX., and Thompson. H.: Mesothelioma ot i
Pleura and Peritoneum Following Exposure to Asbestos in the '
London Area, Brit J Industr Med 22:261-269 (Oct) 1965.
*'
14. Selikoff. I.J.. et al: Asbestosis and Neoplasia. Amer J Med [
42:487-496 (April) 1967.
i\
k- -
Many, possibly most, of the words in the dictionary
stand there as representatives of a whole family of forms.
Not even the timidest of the linguistically timid will run
to the dictionary for encouragement when, for instance,
they want to refer to a spell of "hiccuping," provided they
are certain that Webster does know "to hiccup."
All the tense forms, the participles, the gerunds are assumed to be authorized
by implication the moment the infinitive is known to exist. The plurals of nouns
are similarly taken for granted, and the forms of comparison and the adverbial
forms of adjectives.
This phenomenon is generally covered bv the assertion that a dictionary is not
a grammar and that each individual entry in a dictionary stands simultaneously
for all its grammatically possible forms. (For details, consult your grammar.)
But is a gerund a grammatical form? Or is it a suffix-derived noun? ,
I am not really looking for an answer. I ask-those questions to suggest that the
dividing line between grammatical form and derived neologism is both hard to de
fine and artificial. If I distinguish--among men--the "hunting" from the "hunted,"
I have done no more than form (grammatically) two nouns from two adjectives
which are forms (grammatically) implied in the existence of "to hunt." But if
"hunting" is implied, why not "hunter"? Why not "huntee" and "huntable" and
"huntabiiize"?
The question of when a new word is a new word and when it is merely an "im
plied" form of a conventional term is indeed more complex than is grossly ap
parent. Take "dehairabilitv" as an example. Can I claim the word is implied in
the existence of "hair," or must I assume the responsibility for having spawned
a monster?
Or take "unequivocably," which indeed was the starting point of all this rea
soning and wondering, for it was spotted as a bold neologism in JAMA in the
sentence, "Research at the Public Health Service Hospital at Lexington, Ky, has
unequivocably proven that methadone has all of the euphoric properties of
morphine. ..."
. 1
Now, clearly, the adverb "unequivocably" is grammatically implied in the ad
jective "unequivocable," and this in turn is implied--grammatically of semi-gram-
matically or otherwise--in "equivocable." If we grant further that formations in
"-able" of "-ible" are likewise legitimate without special dispensation, we shall
conclude that "unequivocably" is in no sense a bold departure since "to equivo
cate" is a firmly established, standard English word.
But there is a hitch and a flaw in the argument. "To equivocate" means "to
use ambiguous language" and (by extension) "to render ambiguous." Hence,
"equivocable" can only suggest the trait of "being apt or able to be made ambig
uous," and that, I fear, was not intended. Which means, by (nongrammatical)
implication, that the discrepancy between the obviously intended meaning of "un
equivocably" and its structurally supported significance was the cause of the un pleasant jolt experienced by the spotting reader.
PS.--It is of course possible, and even likely, that "unequivocably" was just a
typo for "equivocally."
500^0^47
Alexander Gode, PhD
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and mende
Ii tablished b; ing is the d . presentatior simple reces
i Case 1. (JI f 1!M7. The pr
complications, f. from birth. I:
1-. l. .y rec_ eived . d From the Div
doe. Johns Ho
/- School of MedicPi the College of I ' Reprint reque:
ji; (Dr. McKusick).
no JAMA, April 8, 1968 Vol 204, No 2 i
iracury infec-
.Sliiilcv Hudson
'
:
s
It
S. csiler3 EA: .u* of histamine Environ Health
and its possible Envhon Health
iciwnson MR. t=t ry failure in a \onia. Amer Rev
jcou3 flow and rats exposed <x> istr Med 13:110-
effect o sulfur : tracbea in vivo -.1 capacitv ol the 366-567,1961. ifc QN: Nitrogen resistance in al*eatth 20:303-309,
l/.mars KS. et 1: cells. Arch En;:i-
.'oa DL: Effects cell population. .I
vs influencing the .g. J Clin Invest
-rial clearance in' American Soci-
-h)
of aerosols upon a pies to sulfur :c Q 13:149-155,
The effect o vannea pigs to sulfur 9-1X5,196S. .'raisal of paiticullfuvic acid. / Air
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Carcinogenicity of Amosite Asbestos
Irving J. Selikoff, MD; E. Cuyler Hammond, ScD; and Jacob Churg, MD, New York
'
Few data exist concerning the comparative neoplastic potential in man of the several kinds of asbestos. In particular, there has been no evi dence concerning whether the amosite variety is carcinogenic. The matter is ci practical im portance, since amosite use in the United States has sharply increased. The mortality experience of a group of 230 men previously employed in an amosite asbestos factory was studied during the years I960 through 1971. Total deaths were more than twice the number anticipated: 46.4 were expected, and 105 occurred. Some 14 deaths were due to asbestosis. Both lung cancer and mesothelioma were found in considerable ex cess. Two or three deaths from lung cancer were expected, and 25 occurred. There were five deaths from mesothelioma. Occupational exposure to amosite asbestos can be associated with serious cancer hazard; its continued industrial use re quires rigorous control.
ossible differences in the disease potential of the several common, commercially avail able varieties of asbestos fiber (chrysotile, amosite, crocidolite, anthophyllitc) have been sought, since the use of asbestos might be guided accordingly.1 Experimental studies were undertaken to seek such information. These have not indicated any critical differ ences; mesothelioma can tie produced easily by intrapleural inoculation of various types of asbestos.2 There is less information concern ing experimental lung cancer.3
Submitted for publication Feb 7, 1972: accepted March 17.
From the Mount Sinai School of Medicine, City University of New York, and the American Caneor Society, New York.
Reprint requests to Department of Community Medicine, Mount Sinai School of Medicine, City rjnivers.ty of New Yosk, Fifth Ave & 100th St. New York, NY 10029 (Dr. Selikoff).
Few data exist concerning the compara tive neoplastic potential of the several kinds of asbestos in man. Some information is available for chrysotiio,-* crocidolite.3 and anthophyllite.3 However, there has been no evidence to indicate whether or not the amo site variety is also carcinogenic.
In large part this has been the result of epidemiological difficulties. Since there is often admixture of fiber varieties under in dustrial circumstances, the experiences o: employed populations are not always readi ly attributable to a single fiber variety. Dili gent efforts have been made to investigate the occurrence of disease in the Transvaal in Soutit Africa, the only area in which-amo site is mined, and where populations ex posed only to amosite could be identified. Environmental studies in this area, reported in 1964, showed no instance of mesotheli oma in amosite miners and only isolated instances of carcinoma of the bronchus, al though asbestosis was found.7 This survey has since been complemented by a study of miners in the area. No attempt was made to study the Bantu workmen who are in die maioritv, since labor turnover is very high, and ". . . records kept are such chat foliovv; up of individuals over a period of time is* impossible.''3 The fate of white miners em ployed between 1954 and 1558 was investi gated. Unfortunately, the records turned out to be imperfect and incomplete, since the white work force in these mines was unsta ble. Only 147 white miners could be fol lowed at ail. and only 20 of these were observed for more than 20 years after first exposure to asbestos. Among these 20. there was one instance of lung cancer and none of mesothelioma. Elsewhere, comment is made
Arch Environ Health.--J/ol 25. Sept 1972 .
500*10237
184 AMOSITE ASBESTOS & CANCER--SEL1K0FF ET AL
that ``The position of amosite is not clear , . with only one pleural mesothelioma stated to be known in the Transvaal.9
Increasing Use of Axnosite in the US
Whether or not amosite is carcinogenic is of some practical importance. Because this variety of asbestos has not been reported to cause cancer, there- has been a tendency in Great Britian, for example, tc substitute it for other kinds of asbestos, especially crocidolite. Moreover, increasing amounts of amosite have been sent to the United States from South Africa. There is no record of amosite being imported before 1930, and as late as 1940, only small amounts were re ceived. Since the Second World War, the situation has changed. Annual imports have risen from less than 500 tons in 1935 to 4,500 in 1945, 18,000 in 1955, and 21,400 tons in 1965 (Table 1).
The US Department of Commerce has reported imports of amosite and crocidolite into the United States (in tons per year) 3s follows:
Total Amosite and Crocidolite
1930
1,907
1931
823
1932 ..................................................... 212
1933
233
1934" ..................................................... 152
1935
501
1936 ..................................................... 1.432
1937
2,928
1938
3.282
1939
6,129
These data should be considered with appreciation of the long-lapsed period be tween onset of asbestos exposure and ap pearance of asbestos cancer--usually 20 to 30 years-or more.10 Cancers that may be associated with the amosite now being im ported-will not become clinically evident until the 1990s or after the year 2000.
Current Investigation
We have investigated the mortality experi ence of a group of workmen occupationally exposed solely to amosite whose employment started between June 1941 and December 1945. This cohort has been observed through June 30, 1971.
Employed Population.--Nine hundred thirty-
three men were employed for varying periods
of time in an asbestos products factory in an eastern city of the United States, starting work some time between June 1941, when the facto-
ry began production, and December 1945. The plant continued production until November 1954, when it closed its doors. It manufactured amosite asbestos insulation, primarily for use in
shipbuilding and ship repair.
We have sought to trace each or these men and have successfully done so in 868 instances
so far (93%). In 65 instances, tracing is still incomplete. Data concerning date of birth, on set of employment, duration of employment,
and type of work are known. For the purpose of this report, we have
investigated the mortality experience of those individuals who had at least one year of em
ployment There were 333 such men who began work sometime between 1941 and 1945: 88 died by Dec 31, 1559; 15 were lost to follow-up; and
230 were alive on Jan 1,1960, and each of these men has been followed since. Table 2 provides an analysis of man-years of experience for these 230 men, by age category.
We have calculated expected death rates for these men in the Jan 1, 1960 through June.30.
1971 category, using age, year, and sex specific rates for US white men. Expected deaths were
then compared with those observed. - -
Amosite Exposure.--No information is avail able concerning dust levels in this plant. Al though exhaust ventilation was used,- discus
sions with surviving workmen and plant man agement indicate that dust exposure, at least in some circumstances, could have been high. Res
pirators were issued to the work force but
were inconsistently used.
.
We have ascertained that or.lv amosite asbes tos was used in this factor,' in several ways;
1. Review with plant management indicated that, only this fiber variety was purchased and-,
utilized. This is consistent with the ship insu- !
Iation specifications under which the products .
were made.
_
2. We have obtained samples of the products made; examination of these samples by polar
ized light microscopy, electron microscopy,' electron diffraction, and electron microprobe analysis showed only amosite to be present.
3. Asbestos was still present in the factory
building's storeroom. When retrieved and ex amined, the material was found to be amosite,
by employment of the same analytical methods.
4. Several workmen had kept their own res
pirators, dating back to their period of em ployment The filters in these respirators were
studied. Fibers retained on. the filters were
Arch Environ Health--Vol 25, Sept 1972
500^0238
-,'i innif'ir`"rr f
'ii
AMGSITE ASBESTOS & CANCER--SEUKOFF ET AL
185
* varying periods *ts factory in an cs, starting work . when the factoember 1945. The until November It manufactured manly for use in
; ! ; i s ! L
ch of these men in 868 instances
tracing is still late of birth, onof employment,
.
report, we have crience of those one year of emmen who began .nd 1945: 88 died o follow-up; and ind each of these Table 2 provides
experience for
.
! death rates for
i hrough June 30, and sex specific
:ted deaths.were -
ved.
-mation i3 avail-
this plant. Al-
is used, discus-
and plant man-
.'sure, at leastJn-- ! -
--
been high. Res-
work force but
Table 1.--Estimated US Asbestos Fiber Consumption (Tons)
Year 1920 1925 1930 1935 1940 1945 1950 1955 1960 1965-
CroeidoKte No data No data
8,700 8,500 11.700 19.600 IT. 100
1.907* 5C1*
8.068*
Amosite No data No data
4,500 5,400 18,000 19.500 21.400
Canadian Chrysolite
152,000 200.700 19S.200 154,200 225.900 355,300 687,400 699,100 605,800 661,100
Other 4,000 4.100 3.500 20.500 36.300 9.000 27.400 11.600 24,600 20.100
Total 156,000 204.800 208,407 175.201 270,268 378,000 723,700 740.400 665,530 719.700
* Amosite and crocidotite combined; not separately recorded.
Table 2. --Man-Years of Experience Among 230 Amosite Factory Workers
(1/1/60--6/30/71)
-
Age Under 40 40-44 45-49 50-54 55-59 60-64 65-69 70-74 75-79 80-84 85+ Total
Jan 1, 1960 Through
Dec 31, 1964 471.7 528.8 501.9 415.2 347.3 285.2 198.4
204.0 89.7 38.0 8.0
3088.2
Jan 1,1965 Through
June 30, 1971
54.8
438.3
619.5
. 565.2, , .
472.2
352.4
272.9,.,
.
163.9
134.1
47.0
..
25.0
3145.3
.
y amosite asbesverai ways: -ment indicated - purchased and i the ship insu-h the products
of the products -nples by polaron microscopy, 'on microprobe he present
in the factory crieved and ex1 to be amosite, lytical methods, t their own resperiod of emresnirators were he filters were
_
Table 3.---Causes of Death Among 230
.
Amosite Asbestos Factory' Workers (1/1/60--6/30/71)*
Cause of Death
Observed Deaths
Expected Desthst
Total cancer, all sites
43 3.5 .
Cancer of lung, pleura, broncnus. trachea
27 2.4 .
Lung cancer
25 . ..
.
Pleural mesothelioma
2
Peritoneal mesothelioma
3.
J
Cancer of stomach, colon, rectum
5 1.6
Cancer of alt other sites
s 4.5
Asbestosis All other causes
14 5 48 37.9
Total deaths
105 46.4
* Analysis of lifetime work experience indicates that, for large ma|onty, this was only occu pational asbestos exposure.
t Expected deaths 1950-1964 are based on US age-specific rates for white men in 1962. For 1965-1971, rates for 1968 were utnizec. Smoking habits are disregarded.
{ US data not available, but figure should oe only slightly less than 2.4.
t US data not available but these are rare causes of death in general population.
Arch Environ Health--Vol 25, Sept 1572
500^0239
7*
wv .!W.1n
11 ^ ! y1:
I s
! i )
l i r
( l [ :
7.
1 1
!
1 i 1 .f f<t * t 1
f (t i \
1 186 AMOSITE ASBESTOS & CANCER--SEL1K0FF ET AL
removed and analyzed. They were Invariably amosite.
5. We have extracted mineral fibers from the lungs of individuals in this cohort who had died. Large numbers of fibers were present. Electron diffraction and electron microprobe analysis showed them to be amosite,11 except for the occasional chrysotile fibril expected to be present in the lungs of urban dwellers in this area.12
anticipated that 2.4 deaths from lung cancer would eventuate; 25 occurred. The calcula tion of expected rates disregarded smoking habits, since the smoking habits of individu als not examined by us are not accurately known. In prospective studies from this point on, smoking habits will be taken into account.11
Mesothelioma caused five deaths: two
Results
pleural, and three peritoneal. Each has been histologically verified in material obtained
The mortality experience of this group of workmen, 1960 through 1971, demonstrates that a serious health hazard was associated with this industrial use of amosite. Table 3 records expected and observed deaths.
Total deaths were more than twice the number anticipated: 4614 were expected and 105 occurred. This excess deatn rate was limited to two categories: cancers of various sites and asbestosis.
Fourteen deaths were due to asbestosis, when virtually none was expected. That amosite can result in asbestosis has been previously recognized.7 In physiological studies of a select group of workmen at this particular factory from 1954, serious pul monary insufficiency had been demon
during operations in two instances and at autopsies in three. In one case, there had been prior chrysotile exposure; in four, only amosite asbestos exposure had occurred. Parenthetically, additional instances of meso thelioma have occurred among men working in this plant, other than in the cohort re ported here.
It may be of interest that more deaths from cancer of the stomach, colon, and rec tum have occurred than expected. The in crease is only threefold, however. As with similar previous experiences, further obser vations are required before this association can be regarded as clearly established.13
This investigation has been supported in part by research grant ES 00358 ot the National Institute of Environmental Health Sciences, US Department
*
strated.13
of Health, Education, and Welfare.
Both lung cancer and mesothelioma were
Field investigations were carried out by Dorothy Perron, Shirley Levine, Ravla Margolies, and Charles
also found in considerable excess. It was V. Nolan.
References
4 L "Whipple HE (ed): Biological effects of asbes
8. Sluis-Cremer GK: Asbestosis in South African
tos. Ann NY Acad Set 132:706-721, 1965.
asbestos miners. Environ Res 3:310-319, 1970.
2. Wagner JC, Berry G: Mesotheliomas in rats
9. Wagner JC: Asbestos cancers, editorial. J Nat
following inoculation with asbestos. Brit J Cancer Cancer Inst 46:v-ix, 1971.
23:567-581, 1969. 3. Smith WE, Miller L, Churg J: An experimen
tal model for study of co-carcinogenesis in the respiratory tract. Oak Ridge, Tenn, Atomic Energy Commission symposium series 21, 1970, pp 299-316.
4. McDonald JC, McDonald AD, Gibbs GW, et al: Mortality in the chrysotile asbestos mines and mills of Quebec. Arch Environ Heahh 22:677-636, 1971.
5. Wagner JC, Sleggs CA. Marchand P: Diffuse pleural mesothelioma and asbestos exposure in the North Western Cape Province. Brit J [ndustr Med 17:260-271, 1960.
6. Kiviluoto R. Muerman L: Results of asbestos exposure in Finland, in Shapiro HA (ed): Proceed ings of International Conference on Pneumoconiosis, Johannesburg 1969. Capetown, South Africa, Oxford
10. Selikoff IJ, Bader RA. Bader ME. et al:
Asbestosis and neoplasia, editorial. Amer J Med
42:487-496. 1967.
.
.
11. Langer AM. Rubin I, Selikoff IJ: Electron
microprobe analysis of asbestos bodies, in Shapiro
HA (ed): Proceedings of International Conference
on Pneumoconiosis, Johannesburg 1969. Capetown.
South Africa, Oxford University Press, Inc, 1970, pp
57-69. .
-" ' '
12. Langer AM, Selikoff IJ, Sastre A: Chrysotile asbestos in the lungs of persons in New York City. Arch Environ Health 22:348-361, 1971.
13. Bader ME. Bader RA, Selikoff IJ: Pulmonary
function in asbestosis of the lung: An aiveolarcapil-
lary block syndrome. Amer J Med 30:235-242. 1961.
14. Selikoff IJ. Hammond EC, Churg J: Asbestos
University Press, Inc, 1970. pp 190-191.
exposure, smoking, and neoplasia. JaMA 204:106
7. Sluis-Cremer GK: Asbestosis in South Africa: 112,1968.
Certain geographical and environmental considera
15. Selikoff IJ, Churg J, Hammond EC: Asbestos
tions. Ann NY Acad Sci 132:215-234,1965.
exposure and neoplasia. JAMA 188:22-26,1964.
Arch. Environ Health--Vo? 25, Sept 1972
500^0240
y.i1 fj.g1
w-.%t*Ur1mxjm-ji.njx* ' *