Document RpvKgbrj752kV4Bk69zM6re9a
I in iinmncnlnl llcnlili l`> m/ici inn \HI. .<!. />/>. I II. IVtiO
Epidemiology of Asbestos-Related Diseases
by R. A. Lemen, J. M Dement,t and J. K. Wagoner!:
Hiis paper is intended to gi\e the reader an overs ien of the epidemiology of asbestos*related diseases and Is restricted to priinaril) occupational exposure studies. However, some mention of nonoccupational exposures are made because of their direct relationship to a worker or to a secondary occupational source.
Cher 100 epidemiological studies are reviewed, dating hack to the first case of asbestos-associated disease reported by Montague Murray in 1906. The studies are divided by specific fiber type and by specific disease outcomes and the interaction of asbestos and cigarette smoking is discussed in great detail.
S Introduction
This paper is intended to me the render nn over view of the epidemiology of'asbestos-related dis eases and is restricted to primal ily occupational exposure studies. However, some mention ofnonoccupational exposures is made because of their di rect relationship to a workci or to a secondary occtiIpational source.
Nonmalignant Respiratory Diseases
Historical Studies
The use of asbestos dates back thousands of years:
(however, the modern industry dates from about |SS0. when it was used to make heat and acid icsistant fabrics (/, 2). With the increasing use of asbestos materials, reports ol asbestos-related dis ease emerged. The first record of a ease of asbestosis was re-
Iported in Fngland by Montague Murray in I9()n. Holfman (T) reported t I9IX) that it was the practice ofAmerican and Canadian insurance companies not to insure asbestos workers due to unhculthful condi-
tions in that industry. Pancoast et al. (*/) commented
on x-ray changes resembling pneumoconiosis in 15
individuals exposed to asbestos. The first complete
description of asbestosis and of the "curious
bodies"' seen in lung tissue appeared in 1927, when
Cooke (5) repot ted on a case of asbestosis, and Mc
Donald (A)'reported on the same and another case,
fiach author gave reasons for believing that these
"curious bodies" originated from asbestos fibers
that had reached the lungs. Mills (7) reported the first
case of asbestosis in the United States in 1950. and in
the same year. l ynch and Smith (8) reported on
"aslvcsiosis bodies" found in the sputum of asbestos
workers. I"Ferruginous bodies" is a more descrip
tive term, as other inhaled fibers, c.g., fibious glass,
may also become iron-coated.) Fairly studies led
many investigators to conclude that people exposed
toasiiestos dust developed the disease "asbestosis"
if the dust concentration w as high or their exposure
was long (9 /2).
Kpidemiolojjic Studies
llanies (11) reported that, although fiist impicssious would lead one to believe that only workers continuously exposed to asbestos are at risk of de veloping asbestosis. further consideration of the in dustry and processes should have suggested that many other workers were also at risk. For example, some trades worked in confined spaces where asIvstos was used. Work in shipboard trades was ac cepted by the Pneumoconiosis Panel of the United Kingdom as associated with asbestosis.
February
'Nation'.il
I1n9s8ti0tute
t'wr
Oi.viipalnin.il
Safely
a ml
lleallli.
Imliiv
trj- Wide Studies Uianeh. Koheit A t all I aKuaioiies. 4b7fi Col
nmhia Parkway. Cincinnati. Ohio 4V7<\.
tNIOSH. Division of Kcspiratoty Disease Studies. Morgan
lawn. West Virginia.
tllnvirontnenlal Defense Inml. W ashington. DC.
1
Murphy et ;il. (//) lound thul asbestosis was II
limes as common among pipe insulators involved in new ship construction as among a control group. Aslxrstosis IiiM appeareil 11 years alter exposure or at about h() mppcl-yeais. I he prevalence was 2K' '< after 20 years. They also reported a case of extensive pleural calcification in a worker whose only know n
nsliestos exposure was during sanding asphalt and vinyl tile doors 05).
I.orimer et al. 06). in a study of brake repair anil maintenance workers exposed to asbestos, found that 25r/r of the workers showed evidence of x-ray abnormalities consistent with asbestosis. One quar ter also hail restrictive pulmonary function test findings. Meurman et al. 07) found a three-fold risk ofdyspnea and a two fold risk .-I cough for asbestos workers as compared with controls.'after adjusting for smoking.
Weill et al. (/<S'l reported a decreased lung function in relation to increasing cumulative dust exposure in a group of asbestos cement manufacturing workers. Ayer anil Burg(/9) reported a decrease in pulmonary function in asbestos textile workers with less than ten years of exposure.
In a study of 222 former .insulation plant em ployees. SelikolT (20) reported positive x-ray 11 nil ings among individuals ha\ ing exposures to asbestos
known to be as short as one day. More recently. Anderson et al. (2/1 reported x-ray findings consis tent with asbestosis in household and family mem bers having no known exposure to asbestos other than residing with ajsiiown asbestos worker. These two studies demonstrate the presence of asbestos disease iti the absence of continuing new known exposures.
Wagoner et al (22) demonstrated a significantly increased risk of death from nonmalignant respira tory disease and for diseases of the heart, which in part were secondary to pulmonary disease, among a cohort of workers in a major manufacturing complex using predominantly chrysotile. Among those work ers observed 20 or more years after onset of em ployment. a fourfold increased risk of death due to nonmalignant respiratory disease was observed. Turther evaluation of these deaths revealed that the majority occurred within one year alter termination of employment and at an average age of 52.K years.
Ncwhouse (22) lcported an increased risk of death from nonmalignant respiratory disease in male asIvslos textile and insulation workers with low to
moderate exposure. F.nlerlinc and Henderson (2-2) reported that for all
ages, only IS deaths from asbestosis occurred in several asbestos plants studied from 1941 to 1969. It is significant to note, howev ei. that the stale of New Jersey alone, in the yeais 1969 |9?(). h:til awarded
woikman's compensation for asbestosis to woikers from one of the plants in the study (25.
SelikolT(20) reported a significant excess of dea due to asbestosis among a group of workers in ITS. and Canada. Out of 17.000 asbestos insulai ^ workers, there were 119 observed deaths attribr.to asbestosis. Although it was not reported, the; peeled death rales from asbestosis in the gene population would be virtually zero.
Description of Asbestosis
Asbestosis is a chronic lung disease due to * inhalation of asbestos fibers and is characteri/etf diffuse interstitial fibrosis, frequently associawith pleural fibrosis (thickening) or pleural calcify lion. The characteristic x-ray changes of asbcsti are small irregular opacities in the lower and mid lung fields, often accompanied by pleural thicken1 and pleural calcifications.
The pulmonary librolic changes develop sle over the-years -- often progressively even with further exposure -- and their radiographic detect is a direct correlate of their extent and profusion some cases, minor fibrosis with considerable spiratory impairment anil disability can be prewithout equivalent x-ray changes. Conversely, tensive radiographic lindings may be present v little functional impairment.
Commonly found in asbestosis are pulmon rales, dy spnea, finger clubbing, and cyanosis, any or all.can be absent in any one case. Pulmon: hypertension is frequently associated with advanx asbestosis, and the resultant cor pulmonale (rit sided heart failure) may be the cause of death.
Carcinogenicity
(Xx'iipsitional Exposure: Historical Studic
In 1925. 55 years after the start of large-scale us: of asbestos in industry, suspicion of an associat between asbestosis anil lung cancer was reported 1 ynch and Smith (27) in the U.S. and by (iloyne< in the U.K. About It) years later, case reports pleural and peritoneal tumors associated with Ivstos appeared (29-2/). Epidemiologic cvidei from Doll (22),,showcd a tenfold excess risk of 1) cancers in those U.K. -asbestos textile workers w had been employed before 1920, before rcgulatii' produced improved dust conditions in factori* Similar lindings were reported in the U.S. in l9` Mesotheliomas were also detected, but this fact u not published until later (22. 54). Possible variatiff in risk w ith different types of fiber were rarely co sidcred in (lie early reports. Since 1964. following!1
2 Environmental Health Perspecti'
455 recommendations of the UK'U Woikmg Gump on
6). Asbestos Cancers (IJICC l%s) (.C) r,,, M(u|k.s
tths there has lieen an expansion ofepidemiologic simlies
the r in many parts of the world.
tion
ted exral
Epidemiologic Studies: Lung Cmiccr, Pleural and Peritoneal Mesotheliomas
Mixed Types of Fiber. In most industrial pro
cesses different types of fiber are mixed, so that pure
exposures to a single asbestos type are rare. Mortal
i he hy
led ca-
>sis die mg
ity studies of defined populations of asbestos manufacturing. insulating and shipyard workers have provided the most concrete evidence concernjng the association between bronchial cancer, pleural, and peritoneal mesotheliomas and exposure to asbestos. Reports have come from several coun tries: England (36, 37), Germany (diS'l, the United States (39), The Netherlands (JO), and Italy (41).
w|y
Ollt ion In
Elmes and Simpson (42) have extended their ear lier report (37) to include deaths occurring since l%5 through 1975. The mortality trend has shifted from a preponderance of asbestosis and gastrointestinal deaths to malignancies from lung cancer and meso
t thelioma, diseases associated with longer latent periods. These authors report their findings would
'ilh
suggest any standard based "on the prevention of asbestosis may not provide adequate protection
ary
Imt i.iry
against neoplasia." A sevenfold excess of lung cancer w as found in a
group of insulation workers whose exposures had
ced :ht-
been to chrysotile and amosite. but not crocidolite $). Enterline and Henderson (24) reported a 4.4 times increased risk of respiratory cancer mortality
among retired men who had worked as production or
maintenance employees in the asbestos industry and
who had been exposed to mixed libers. Among men
with mixed exposure to crocidolite and chrysotile in
.'S the asbestos cement industry, the rate was 6. I times theexpccted rate. In a British naval dockyard popu
lation, Harries (44) showed that there had been a
steep rise in mesotheliomas since 1964. However,
the full biologic effects of asbestos in shipyard work
ers would not have been expected to be detected
until the I970's and thereafter (20).
Edge (45) reported that shipyard workers with nee niixedlisbestos exposure and pleural plaques (with ung out evidence of pulmonary fibrosis) had a 2.5 times
-vho increased risk of developing carcinoma of the bron ions chus. when compared with matched controls ies. without plaques. In a study of sheet metal workers >61. (46) with measurable and mixed asbestos exposure, was an excess of deaths from malignant neoplasms
<>ns (24.797 of deaths for two cohorts selected for 5 or mi- more years worked in the trade. 19. Ir; of deaths fora
the group with death claims where 14.5' 7 was expected)
was kneels ullnhulcd to an excess of maliunaut tumors of the icxpiialoix tiact. Ot the 707 deaths in ihe first cohort. 12 lung cancer deaths were signifi cantly in excess 11.7 times the expected). ()ne pleural mesothelioma was observed.
Additional confirmatory evidence of the associa tion between mesotheliomas ami past exposme to asbestos comes from many institutes and depart ments of pathology and cancer registers (47-54). These studies have shown an association between asbestos and mesothelioma even with exposures as brief as one day: however, approximately 1597 of the mesotheliomas are not known to he related to ex posure to asbestos. Three studies (50. 55.56) showed a poor correlation between certified cause of death and histologic diagnosis of mesothelioma. There is still a need to reduce the inter-observer variation in the diagnosis of these rare and pleomorphic Illinoi s (57).
The ratio of pleural to peritoneal tumors appears to be associated w ith heavier exposures (5tf). Among a number of occupationally exposed groups studied, approximately 5-797 of deaths have been from mesotheliomas (20. 59, 60). More recently, however, anestimate has projected that 1197 of asbestos work ers' deaths in Himiand will be from mesotheliomas (61). "
Weill el al. (62) reported on the mortality experi ence of a cohort of 5.645 men employed in produc tion of asbestos cement products and who had at least 20 years since first exposure. These workers were exposed largely to chrysotile with some crocidolite and amosite. Among this group. 601 per sons w ere identified as deceased by the Social Secu rity Administration. Those with unknown vital status (2597) by this source were assumed alive, thus likely resulting in underestimation of the true risk. Death certificates were obtained for 9197 of the known deaths. Dust exposures were estimated using each worker's employment history in conjunction with historical industrial hygiene data.
Weill et al. 162) observed increased respirator} cancer moi lalily only among those with exposure in excess of 100 mppef-yr. where 23 cases were ob
served versus 9.3 expected. The unusually low SMR Tor all causes in the low-exposure groups suggest thus lhe possibility of a selection bias and any in terpretation of risks at low exposures should be done with caution. Two pleural mesotheliomas were re ported. Separating the cohort by type of fiber ex posure. the authors concluded that the addition of crocidolite to cluysotile enhanced the risk for re spiratory malignancy: however, an excess risk was observed among those not exposed to crocidolite w ith cumulati\e exposures in excess of 200 mppcf-
mouths. Both average concentration of exposure
ives February 19X0
3
and duration of exposure were found to be related to cancer risk.
Ben v et al. (6.1) extended the 1968 observations In including persons completing 10 or mote years em ployment by 1972. Persons who left alter June 30. I%(>. were also contacted ami encouraged to partici pate with 6X of 113 persons eventually participating.
Outcome measures studied included chest radio graphs, medical examination including assessment of basal crepitations and pulmonary function (1KV. KVC\ I RC. l ie Rl . I I.. I'aCOj).
Chest films were read by four readers by the II.O/UC 1071 classification system with readings being averaged. Dust exposures were estimated for each person using available hyiene data and esti mates of control effectiveness, m this study, "possi
ble asbestosis" was diagnosed based on one or more combinations of basal rales or crepitations, radio logical changes, a falling transfer factor, and restric tive lung function changes. Among these 379 men. 60 cases of possible asbestosis were diagnosed by the factory medical officer, whereas 83 cases were diag nosed by an independent clinician. Collaboration by these investigators subsequently resulted in 82 men with crepitations. 58 "possible asbestosis." and 34 certified ashestosis. Using the exposure data these authors estimated the cumulative dose necessary for a I9f incidence for crepitations, possible asbestosis, and certified asbestosis to be 43 fihcr/cnr'-yr. 55 fibcr/cm:1-yr. and 72 fihcr/cnv'-yr. respectively. These authors point out limitations of the cumulative dose concept and acknowledge the imprecision of their exposure estimates. Two cases of certified as bestosis w'ere observed among nonsmokers and nine among ex-smokers. There were, in general, fewer respiratory symptoms and signs in nonsmokers and light smokers than in heavy and ex-smokers.
Baselgu-Monte and brancis' examination (64) of 1262 workers employed in four factories in the Bar
celona area demonstrated a dose-response relation ship based upon radiologic images. The authors
demonstrate a quick response for pleural radiologi cal changes at individual cumulative doses as low as 5 flher-year/cnr' while the pulmonary and pletuopulmonai y responses tend to appear later but not at statistically different doses. The authors are reluc tant to draw- conclusions because of the design of the epidemiologic evaluation which considered only ac tive employees. Other epidemiologic studies of wot ker populations would indicate that evaluation of only active employees would tend to underestimate the health risk since diseased workers oftentimes tend to self-select out of the active workerforce (65-67). Baselga-Monte and biancis conclude that "the present worldwide trend to establish more ex igent hygienic criteria lor exposure It' asbest(os) is
confirmed". Based on their working model this k,( 1
for a 50-year working life should be 0.07-0.
liber cm ', "(taking into account protection level' '
99 and 95- ;
'
( rociilotitr. In 1956. Wagner started investigJ
ing the occurrence of pleural and peritoneal rites'
theliomas in the crocidolite mining areas of 0
Northwest Cape Province in South Africa. It "I
shown that these tumors occur fed in the non-mini*
population living in the vicinity, as well as a mol
men working in the mines and mills and in the trail
portation and handling of the fiber (6<S). Asbesto*
was not invariably present. The latent period N
tween first exposure and clinical recognition oft*
tumor w as long -- a mean of 40 years. Subsequc*
surveillance of the mining population in all tf
aslvstos-puklucing areas in South Africa has add*!
support for a major difference in the incidence*
mesotheliomas within the crocidolite mining areas*
that country (69, 70). The mining of crocidolite!
northwest Australia has been associated wit'
mesotheliomas (71). Jones et al. (72) have reported
high incidence of mesotheliomas among women wl'
w'orked with crocidolite in a factory producing d'
mask canisters during World War 11.
'1
McDonald and McDonald (75) have also studif
the mortality of 199 workers exposed to crocidoft1
during gas mask manufacture in Canada during 19!
to 1942. This cohort was followed through 1975 aC
56 deaths occurred. Out of these 56 deaths, four (7*1
were from mesothelioma and eight (1497) from lu*
cancer. This was compared to 0.269f mesotheliotf
deaths among chrysotile miners and millers (
Canada. It should be pointed out that an addition!
five mesotheliomas not reported on death certtf
cates were diagnosed on review of pathology <
autopsy material.
;
C.hrysiitile. McDonald et al. (55 . 74) reported*
increased risk of lung cancer among men employ#
in Quebec chrysotile mines and mills. The risk*
lung cancer among those workers most heavily e|
posed was live times greater than those least e*
posed. These same chrysotile miners and millers!
Quebec as of 1977 hail experienced nine confimrf
and two suspected mesotheliomas (75). The auth(
concluded (75) for the seven cases observed *
Thetford mines that, "There is therefore no gc*1
reason to doubt ghrysotile exposures as the cause.!
Kogan et al. (76) investigated the cancer mortali!
among workers in asbestos mining and milling it
dustries between 1948 and 1967. The total cancj
mortality rate among workers was 1.6 times high!
titan that found in the general male population: If
female workers the rates were 0.8 for those in mint
and 1.3 for those in mills. The lung cancer risk ft
male miners and millers wais twice that of the gened
4 Environmental Health I'erspectbt
1 iliislevcll
male population. loi females in mines ;iiul mills, the
Chrysotile constituted over 99' r per year of the total
.07-0.101 nsks were - * ant* * time's that ni l lie general lemale quantity of asbestos processed, except I'm 3 years
levelsof|, population, respectively. Foi those wotkcis over 50 dm mg Win Id Wat II Dining these 3 years, amosilc
years of age. the risk oflmig cancer was greater: for was selectively used to a limited extent because of
vestigat- men in mining, 4.0: those in milling. 5.0; for women Naval specifications and accounted lor approxi
il meso- in mining. 9.5: and for those women in milling. 39.K mately y.'/ of the total asbestos used per year.
of the limes that found in the general population. No (Tocidulite and amosite for the* other years ac
It was mesotheliomas were found, but Kogan et al. (76) counted for less than V'A of total usage in very
^-mining indicate.that this might be explained by the insuffi selected areas, exposures to these other two types
among cient experience of pathologists with this rare type of may have played a role in the etiology of disease:
c trans- cancer in that geographical area. Also, the number of however, due to the overw helming exposure of the
oestosis people in the study populations was not reported.
cohort to chrysotile it is likely that the other ex
iod be Selikoff(77) surveyed 4S5 current employees of a posures playeil a minor role in the overall mortality
lt of the chrysotile mine in Haire Verte. Newfoundland, patterns. Robinson et al confirmed the observations
sequent which had been in operation since 1963. Kilty em of W agoner et al. of statistically significant excess
all the ployees (lO'/f) had one or more radiographic abnor
s added 8 malities of the type commonly associated with as
deaths due to bronchogenic cancer, suicide, heart disease and nonmaligiiaut respiratory disease, in
ence of bestos exposure. Parenchymal abnormalities were areas of most common while pleural changes were detected lolite in in only of the individuals survey ed. I or those
cluding asbestosis and nonstatistically significant excesses of digestive cancer and lymphoma. Robin son et al. described 17 mesotheliomas, whereas no
d with individuals with less than 5 years employment, the mesothelioma' were detected in the Wagoner et al.
ported a prevalence of abnormalities was 5' '< and this in study w here observation of mortality ceased in 1967.
ten who creased with duration of employ incut. Changes oc The appearance of 17 mesotheliomas in the updated
ring gas curred most commonly in those with the most in- study reflect latency periods of 24 to 53 years since
| tense exposures. This study was designed only to onset of first exposure. Further analysis indicated 3
t'cd cdl ^sess asbestos-related disease under more modern of the 17 mesothelioma deaths occurred during the
cm*/lite ditel conditions than have previous studies (76, 7<V). and original study period hut were undetected until later ng 1939 thus short duration of exposure and long latency analysis. This observation confirms earlier findings
975 and could not he studied. The interpretation of these data by Mancuso and HI-Attar (cHO) that mesotheliomas
nir H%) is further complicated by the lack of a cohort popu are characterized by very long latency periods.
>m lung lation and environmental measurements. The study
Weiss et al. {<HI\ reported no unusual mortality
helionta docs demonstrate the prevalence of chest x-ray Hers in changes in an appreciable proportion of employed
experience over a 30-year period for a cohort of workers employed in a paper and millboard plant
ditional workers despite a sho/t period from onset of initial reported to be using only chrysotile. The author con
certifi- exposure.
cluded that the study results were suggestive of a
dogy or jr^Wagoner et al. (22) reported on the cancer risk minimal hazard from chrysotile. This conclusion
among a cohort of workers in a major manufacturing must be view ed in light of the limitations inherent in
orted an. coniplex utilizing predominately chrysotile asbestos the study. First, the study population was small (n =
nployetyl jn textile, friction, and packaging products. An ex- 264) and only 66 workers had died at the time of
- risk obr'Jessof respiratory cancer occurred among asbestos analyses. Moreover, the unusually low SMR for
ivily ex workers in each duration-of-employment category many of the contrasts in t-he W'eiss et al paper sug
east ex- down to and including 1-9 years. They observed gests the possibility of a selective bias greater than
[s of I statistically significant standard mortality ratios of eeddl |22 for all malignant neoplasms and 244 for malig-
usually seen in contrasting industrial populations with the general population.
uihhoorrl mint neoplasms of the respiratory system. The as
Hntcrline and Henderson (24) found that for re
i ved at bestos workers in this study were located in an area tired men who had worked as production or mainte
io good of predominately Amish Dutch population with nance employees in the asbestos industry and who
ause." known low frequencies of smoking. The authors, had reached 65 years of age. those who had been
natality nevertheless, used the general white male U.S. exposed only to chrysotile had a respiratory cancer
lling in population as a control group, which would tend to risk 2-4 times greater than that expected. Among
cancer underestimate the degree of risk.
men within the asbestos cement industry exposed
- higher Robinson et al: (79) reported an additional 8 years only to clu v solilc. a one to fourfold excess ot respi
ion: for ofobservation and 3X5 deaths to the Wagoner et al. ratory cancel was found. < )l S()2 deaths, only one
n mines (23) study of mortality patterns of winkers among mesothelioma had been recoiiled in the several
risk for one facility manufacturing asbestos textile, friction plants investigated. In coniiast. a subsequent inves
general ukI packing exposed piedominately to chrysotile. tigation In Hoiow el al. (6/1 found 70 cases ol meso
jk*c lives February 19X0
thelioma from only one ol these plants. The disciepaney was due to methodologic variations, lor ex ample. Fnterline and Henderson l24) had limited their investigation to men ape 63 or over, while many ol the mesothelioma eases leporled hy Borow et al. (67) had died before that ape. xdAcheson et al. (X2) estimateil ash-fold risk of 'mesothelioma for persons with ehrysotilemTlic limp" -.tissue.
Aiimsite mill Anijihilmle hihers in the ('.iiniiniiif;timite -- (lrunerite Ore Series. Lxposurcs to aillOsite alone in a factory making insulation material were reported by Selikoff (20) and Selikoff et al. ifU). Ten mesotheliomas were found in addition to an increased risk of lunp cancer in workers who were observed 20 years or longer. The excess limp cancer risk in the timositc workers was shown to increase with duration of employment. There was a three-fold increase in lunp cancer among those with less than 3 months employment and among those with less than I month employment there was a 2.23-fold increase.
In a retrospective study of 914 men who had worked periodically during World War II in a plant manufacturing insulating materials from amositc for the U.S. Navy. Seidman el al. (<S4) concluded that the group of 65 men who had worked for less than I month had experienced excess mortality, on the agc-spccific basis, from lung cancer during the 30 years since the beginning of their exposures, but not from all cancers or all causes of death. Men who had worked for a full month or longer hail excess mor talities from all three causations examined, the risk ofdcath from lung cancer increasing with duration of exposure.
Seidman et til. (<X3) have extended their study of amosite asbestos workers with short-term expo sures. The study group consisted of 820 men lirst employed between June 1941 and December 1943 in the production of asbestos insulation, follow-up was through 1977 with expected deaths adjusted for ape and calendar time estimated using death rates for w'hite males in the general population of New Jersey.
Among the cohort studied by Seidman et al.. 83 lunp cancel s were observed according to death cer tificate information whereas 23.1 were expected. Among 61 men employed less than I month, three lung cancers were observed versus 1.3 expected. Although based on small numbers, excess mortality from lung cancer showed an increasing tiend with employment duration. Cancer latency periods were progressively shortened with increasing employ ment duration, four mesotheliomas were reported on death certificates in contrast to 14 which were identified on autopsy and other tissue diagnosis. Three in the group had less than 1 year of exposure. Although no environmental data are available for
6
this plant. dust counts were made in another plant of the same company using the same liber type and production process. Seidman et al. reported average exposure at this plant to be 23 fiber/cm'. Further data available for this comparison plant were published by NIOSH t.S'6) showing mean exposures to range from 14 to 73 libers/cc. At such concentrations, a lung cancer relative risk of 2.3 could be calculated with employment less than one month.
Johnson et al. (S7) have documented the hazards
ha ris:
do: exF dy v
me Fin thk
gra
of asbestosis encountered among workers at a plant manufacturing amosite insulation products in Tyler. Otl
Texas. Seven of 18 workers with ten or more years 1 employment at the plant had asbestosis. established pop
by the presence of at least three of five criteria in of i
cluding restrictive pulmonary function, chest x-ray true
abnormalities, rales, clubbing, and significant dysp less
nea. S
Murphy et al. (SH) reported a follow-up to their enif
first report (N) of shipyard pipe covers exposed dos
predominately to amosite asbestos. Workers in the dos
original Murphy report of 1971 with "asbestosis" revi
diagnosed by multiple criteria had a poor prognosis clu.i
reported in the 1978 longitudinal survey. The studies part
of Johnson et al. and Murphy et al. demonstrate the cer.
respiratory morbidity associated with manufacture F
anil use respectively, of amosite insulation products. due Gilliam et al. \89) reported a threefold excess risk ami
of mortality from respiratory cancer and a twofold frie excess of nonmalignant respiratory disease (ex The cluding influenza and pneumonia) among miners ex whi posed to amphibole fibers in the cummingtonite- j;
gmnerite ore series at concentrations less than 2.0 wit: fibers/cnr' and a large majority shorter than 3 gm in kno length. McDonald et al. (W)) in a subsequent study of thn the same mine examined the mortality experience of bee persons with at least 21 years of employment at the Ne> mine which showed significant excesses of pneu oft moconiosis (mainly silicosis), tuberculosis, and Woi heart disease. No overall excess of malignant dis
eases were found: however, when the population No:
was broken down by exposure, respiratory cancel
was in excess. The contrast between the cancer F
findings of the two studies are not surprising since wit
MclXmald et al. looked.only at workers surviving al 12/
least 21 years of employment. Gilliam et al.. on the froi
oilier hand, did not use such a rigid survival crite am< rion. They included all miners with 3 years employ woi
ment underground who had never mined under A
ground elsewhere. The findings of McDonald et al eva do not negate those repotted by Gilliam et al. but disc
rather tend to strengthen them, in that McDonald woI
used rigid survival criteria and further diluted the cast
underground exposed effect by including person1 never exposed underground thus any excesses ma)
fom insu
be underestimated.
son
Hnvironmentul Health Perspective? Feb
nt of and
r;iue data bed mge is. a
atcd
Anihophyllite. In Finland, .lnlliophy Hite mining fiasheen associated with an excess bronchial cancel'
risk of ltimes the expectation oxerall. and about double this figure for those with more than 10 years' exposure (911. There was also a higher prevalence of dyspnea and cough in the mineis. However, no mesotheliomas were found despite the presence in Finland of an unusually high incidence of pleural thickening and calcification as detected by radio
ards graphic and pathologic surveys {92. 9.?).
)lant yler, Other Types of Cancer
ears
shed a in.-ray ;ysp-
Epidemiologic studies of the already defined populations have consistently shown an excess iisk of other cancers, especially of the gastrointestinal tract {22. 27. 58, 74. 76, 80. 94): however, it has been less than that of lung cancers.
'heir used i the isis"
iosis
refs.
> risk '('old (e\-
s ex it itei 2.0 ;m in
Jy of ce of
t the neu-
and : dis-
Schneiderman (95). in a literature review with an emphasis on dose response, concluded that "good dose-response data, with quantitative estimates of dose are uncommon; however, in all the literature ^viewed, only one paper did not support the con clusion that increased exposure to inhaled asbestos particles leads to increased digestive system can
cer." Robinson et al. (79) reported an excess of deaths
due to lymphosarcoma and malignant lymphoma among white males employed in an asbestos textile, friction and packing products manufacturing facility.
There were seven deaths due to cancer of these sites, while 3.28 cases were expected.
Stell and McGill (96) found that out of 100 men with squamous carcinoma of the larynx. 31 had known exposure to asbestos compared with only three in matched controls. Similar associations have been reported by Shettigara and Morgan (97). Ncwhouse and Berry (98) found two cases of cancer of the larynx (ICD 101) in their cohort of over 4000 workers compared with an expected 0.4.
ation
Nonoccupational Exposure
-.
Household contact with asbestos is associated with an increased mesothelioma risk. Anderson et al.
>ng at
n the erite ploy.
ndcret al.
Hut .maid d the 'sons may
Ql) have reviewed 34 such cases of mesothelioma from nine countries and reported lour new cases among the traced family members of 1664 asbestos
workers. Anderson et al. (99) 11979) have continued to
evaluate the risks of nonmalignanl and malignant disease associated with household exposure to work-derived amosite dust. Four mesothelioma cases were reported among household contacts of
former workers at a plant manufacturing amosite insulation products in Paterson. New Jersey. Ander son et al. also reported a 35.9r< prevalence of r.ulio-
giapluc ahnoimalitics among household contacts of former employees at this same amosite plant com pared to a 4.6' I prevalence among a control group. These radiographic abnormalities included pleural thickening, pleural calcification, pleural plaques, and irregular opacities. These studies raise the spectre of nonoccupational ha/ards'associatcd with casual or low-level exposures to amosite. Cases of mesotheliomas have also occurred in nonoccupationally exposed individuals living in the neighborhood of industrial sources of asbestos (,?6, 100. 101). Studies of the geographical distribution of eases of mesothelioma in the UK over a 10-year pei iiul indicate that the new eases are nearly all from areas in which there has been a recognized industrial source of asbestos (50. 102).
Lesions among nonoccupalioually exposed per sons in Finland have been reported where anthophyllite asbestos is mined. In this study, 118 cases of the total 126 cases of roentgenologieallydiagnosed pleural calcification studied, excluding those individuals with hemothorax, emphysema, and tuberculosis, lived or have lived in areas imme diately adjacent to asbestos mines (92). The results of this study suggest a health hazard from commu nity exposure to ambient asbestos.
Synergism
There is marked enhancement of the risk of lung carcinoma in those w oi kers'exposed to asbestos who also smoke cigarettes 1102, 104). Hammond and Sclikoff (66) interpret the excess lung carcinoma risk from asbestos in nonsmokers to be small. No link between cigarette smoking and mesotheliomas has been observed in a prospective study by Hammond and Sclikoff (60). A preliminary study (105) on female workers employed between January 1940 and December 1967 in a predominately chrysotile as bestos textile plant revealed seven lung cancer deaths among 580 women when only 0.63 deaths were expected (p 0.01). One lung cancer death was observed in a smoker, two in women of undeter mined smoking history, and lour in "never" smok ers as determined from hospital admission charts.
It is important to note that the historic documen tation of cigarette consumption patterns is lacking for most retrospective cohort studies of asbestos workers. It is further important to note that a sizable portion of the general population, the group usually selected for comparison in these studies, are cigarette smokers. I hercforc. the risk of lung cancer demonstrated for these industrial groups exposed to aslvstos is of such magnitude as to preclude the identification of an independent etiologic role for cigarette smoking.
vtives j february 1980
7
Hammoml cl al. UOh) have attempted to correct
this methodological problem by comparing 12.051
asbestos insulation workers having complete smok
ing histories to a control population also with no
smoking histories. Hammond et al. used as a control
population 75.765 men from the American Cancer
Society's prospective cancer prevention study who
were similar to the asbestos workers in that they
were white males; nonlarmers; had no more than
high school education; had a history of occupational
exposure to dust fumes, vapors, gases, chemicals, or
radiation; and were alive us of January I, 1%7. Non
smoking asbestos workers showed a five times
greater risk of dying from lung cancer than their
nonsmoking controls, while smoking asbestos work
ers also had a live times greater risk of dying of lung
cancer than their smoking controls. Both smokers
and nonsmokers exhibited a fivefold relative risk:
however, the attributable risk was greater among the
smokers. This higher attributable risk can be ac
counted for by the large number of smokers in the
asbestos-exposed population and the comparison
population.
Liddell et al. (107) has also looked at smoking
lunong asbestos workers through administering a
questionnaire to living workers or relatives of de
ceased workers dying after 1951. The authors report
SMR's of 48 and 46 for nonsmokers and ex-smokers,
increasing to 206 for heavy smokers. This study,
however, suffers since smoking specific death t ales
were not used for calculation of expected lung cancer
deaths underestimating the risks among non
smokers.
None of the epidemiologic studies have shown an
increase of pleural or peritoneal mesothelioma
tunong smokers as compared to nonsmokers.
Conclusion
In addition to the nonmalignant effects of asbes tos, all commercial forms of asbestos have been shown to be carcinogenic in man. and occupational exposure during mining where ashestiform fibers occur also accounted for an excess of cancer in min ers. In addition, household contact with asbestos workers has demonstrated a risk for nonmalignant and carcinogenic effects.
It has been estimated that of the 4 million workers heavily exposed to asbestos, at least 1.6 million (55^1457) are thus expected to die of asbestos-related cancel s, w hile in the absence of asbestos exposure only about 0.55 million (8-9''/) would have been ex pected to die of cancer. Broken down more specifi cally. these cancer deaths include 20-2557 from lung cancer, 7-1057 of pleural or peritoneal mesothelioma, and 8-907 of gastrointestinal cancer. It is estimated
8
that between 58,000 and 75.000 asbestos-associaK deaths will occur each year, which will account f between 15 and ISr7 of the total cancer deaths inf3 United States (108).
REFERENCES
'
1. Hendry. N. W. The geology, occurrences, and major use"
asbestos. Ami- N.V. Acad. Sci. 132: I (19651.
2. Hucpci. W. C. Occupational and environmental cancerso
the icspiratory system. In: Recent Results in Cancer R-
search. Vol. 3. Renlehnick. Ed.. Springer-Verlag. No
York. 1966. p. 38.
3. Hoffman, E. t.. Mortality from respiratory diseases indiisti;
trades (inorganic dusO, Bulletin 231. U.S. Dept, of l.ahx Bureau of Labor Statistics. 1918, pp 176-80.
4. Pancoast. H. K.. Miller. T. (1., and Landis. H. R. M. ;
roentgenologic study of the effects of dust inhalation tipf
the lungs. Trans. Assoc. Am. Ph)sicians 32: 97 (I9I7).
5. Cooke. W. F.. Pulmonary asbestosis. Brit. Med. J. 2: 102-
(1927).
`
6. McDonald. S. Histology of pulmonary asbestosis. Brit Med, J. 2: 1025 (1927).''
7. Mills, R. (i. Ihilnionary asbestosis: report of a case. Mi nr.
Med. 130: 495 (1930).
'
8. l ynch. Is. M.. and Smith. W. A. Asbestosis bodies ri
sputum anil lung. J. Am. Med. Assoc. 95: 659 (1930).
9. Mcrcwether. E. R. A. and Price. C. W. Report on the Effect!
of Asbestos Dust on the Lungs and Dust Suppression in ll*
Asbestos Industry. Her Majesty's Stationery Office. Lon
don. 1930.
1
10. Merewethcr. E. R. A. A memorandum on asbestosis
Tubercle. 75: 69. 109. 152. (19341.
!
11. Fulton. W. B.. Dooley. A.. Matthews, J. L.. and HoutC
R I.. Asbestosis Part II: The nature and amount of dus
encountered in asbestos fabricating plants. Part III: Tin effects of exposure to dust encountered in asbestos fabric*
tion plants on the health of a group of workers. Bulletin 4'.
Department of l abor and Industry, Harrisburg. Pa.. 1935-;
12. Drecssen. W. D.. Dallavalle. J. M., Edwards, T. L.. Miller.
I.W., and Sayers, R. R. A study ofasbestosis in the nsbesto*
textile industry. Public Health Bulletin 241. U.S. Treasury
Dept. Public Health Service. 1938.
\
13. Hanics. P Ci. Asbestos ha/aids in naval dockyard. Anil
Occup. Hyg. 11: 135 (1968).
i
14. Murphy. R. I . IT. Terris. Ci C.. Jr.. Burgess. W. A.. Wor
cester. J.. and (iaensler. E. A. Effects of low concentration!
of asbestos. N. Engl. J. Med. 285: 1271 (1971).
:
15. Murphy. R. I... Levine, B. W.. AIRazzaz. E. J.. Lyncld J. J .and Ituigess. W. A. Floor tile installation as a sourced
asbestos exposure. Am. Rev. Resp. Dis. 164: 576<l9'tl.
16. I oiimei. W. V.. Rohl, A. N.. Miller. A.. Nicholson. W L
and SelikolV. I J. Asbestos exposure of brake repair workert
in the United States, in press.
.
17. Meurman. L. ()., Kiviluoto. R., and Hakama, M. Mortalit)
of employees of anthophy llitc asbestos mines in Finland. In:
Proceedings of the Conference of Biological Effects of Xv
bestos. P. Bogovski. J. C. Ciilson. V. Timbrell. and J. C
Wagner. IARC. Lyon. 1973. p. 199.
.
18 Weill. It.. Ziskind, M. M., Waggenspack. C.. and Rossiter,
C. E. 1 nng function of consequences of dust exposure m
asbestos cement manufacturing plants. Arch. Environ
Health 30: 88 (1975).
.'
19. Ayer. 14.. and Burg. J. Cumulative asbestos exposure and
forced \ ilal capacity. NIOSH internal report. 1975.
20. SelikotT. 1. J. Asbestos disease in the United States I9IS-
1975. Paper presented at the Conference on Asbestos l)ri-
ease. Rouen. Fiance. October 27. 1975.
Environmental Health Perspective
M'CMted I omit for
lis in the
>r uses of
inters of iter Re.
ip. New
industry f 1 .ahor,
M. A
on upon M7|. 2: 1024
s. Brit.
Minn.
'dies in
0).
Effects n in the
How?., of dust II: The ahrica."tin 42. . 1935. Miller, hestos casury
: Ann.
. Worirations
I ynch, urceof '971).
'id. In: of AsI J C.
ssiter, me in i iron.
ie and
191K-
s Dis-
'1 Anderson. H. A., I ilis. R.. Damn. S M . Tischhcin. S . " and Selikofl'. 1. J. Household-contact asbestos neoplastic
risk. Ann. N.Y. Acad. Sci. 271: III (|97h).
r> Wagvjncr, J. K.. Johnson. W. M . and I omen. K. A. Malig
nant and nonmalignanl respiratory disease mortality pat
terns among asbestos production woikcrs. Congressional
Record, Senate Proceedings and Debates. 93id Congress,
First Session. US Govt. Printing Office. Vol. 119. Part 6. pp.
7828-7830 (March 14, 1973). y Newhouse. M. L. A study of the mortality of workers in an
asbestos factory. Brit. J. Ind. Med. 26: 294 (1969).
24 Enterline, P. E., and Henderson, V. Type of asbestos and respiratory cancers in the asbestos industry. Arch. Environ.
Health 27: 312 (1973). is Heymann. R. M. Commissioner, Department of Labor and
Industry. State of New Jersey, personal correspondence,
July 21. 1971. .
.
26 Serraino. C. Commissioner. Department of Labor and In
dustry. State of New Jersey, personal correspondence. September 10. 1970.
27. Lynch. K. M. and Smith. W. A. Pulmonary asbestosis:
carcinoma of the lung in asbestos-silicosis. Am. J. Cancer 24:56 (1935).
28. Gloyne. S. R. Two cases of squamous carcinoma of the lung occurring in asbestosid. Tubercle 17: 5 (1935).
29 Wedler, H. W. Asbestosc und lungenkrebs bei asbestose. ' Deut. Arch. Klin. Med. 191: 189 (1943).
30. Wedler. H. W. Asbestose und lungenkrebs. Deut. Med. Wochenschr. 69: 574 (1943).
Jl. Wyers, H. That legislative measutes have proved generally effective in the control of asbestosis. Glasgow, M. D. Thesis University of Glasgow. UK. 1946.
31 Doll. R- Mortality from lung cancer in asbestos workers. " urit. J. Ind. Med. 12:81 (1955).
33. Mancuso.T. F., and Coulter, E. J. Methodology in industrial
health studies. The cohort approach with special reference
toanasbestoscompany. Arch. Environ. Health6:361196.3).
34. SclikofT, I. J.. Churg. J., and Hammond, E. C. Asbestos exposure and neoplasia. J. Am. Med. Assoc. 188: 22 (1964).
35 UICCWorking Group on Asbestos Cancers. Arch. Environ. ` Health 11: 221 (1965).
36. Newhouse, M. L., and Thompson. H. Mesothelioma of
pleura and peritoneum follow ing exposure to asbestos in the London area. Brit. J. Ind. Med. 22: 261 (1966).
37. Elnics, P. C., and Simpson. M. J. C. Insulation workets in ' Belfast. 3. Mortality. 1940-66. Brit. J. Ind. Med. 28: 226
(1971). 38. Bohlig, H., Dabbert, A. F.. Palguen. P.. Main. F... and Hinz.
I. Epidemiology of malignant mesothelioma in Hamburg.
Environ. Res. 3: 365 (1970).
39. Selikoff, 1. J. Partnership for prevention -- the insulation industry hygiene research program. Ind. Med. .39: 4 (1970).
40 Slumphius. J. Epidemiology of mesothelioma on Waicheren Island. Brit. J. Ind. Med. 28: 59 (1971).
4|. Ruhino. G. F., Seanctti, G.. Conna, A., and Palestro. G.
Epidemiology of pleural mesothelioma in North-Western Italy (Piedmont). Brit. J. Ind. Med. 29: 436 (1972).
4?. Elmes, P. C. and Simpson. M. J. C. Insulation woikcrs in
Belfast. A further study of mortality due to asbestos ex posure (1940-75). Brit. J. Ind. Med. 34: 174(1977).
4). Selikoff, I. J.. Hammond. E C\. and Seidman, 11. Cancer
risk of insulation woikcrs in the United Stales. In: Ptoccedings of the Conference of Biological Effects of Asbestos,
` p. Bogovski. J. C. Gilson. V. Timbreil. and J. C. Wagner, F.ds.. 1AKC. Lyon, 1973, p. 209.
44 Harries. P. G. Experience with asbestos disease and its control in G1e.1t Britain's nasal dockyards. Environ. Res. 11:261 (1976).
13 Edge. .1. R. Asbestos lelalcd disease m Bairow-in-blirness. Lnvnoit. Res II: 244 (1976).
16 Cooper. ('. W Study of sheet metal workers. Final Contract Report. Conti act No HSM-099-71 55. National Institute for Occupational Safely and Health. 1975.
47. Oclajarte. M.. Delajarte, A. Y.. Michaud. J. L. Mesothelioma plcmaux diffus. Etude preliminaire sur 31 cas. Rev. I r. Mai. Resp. I: 697 (1973).
48. Gohbato, F.. and Terri, R. Riccrea epidemiologies sulT incidenza del mesotelioma della pleura nella provincia di trieste. Lavoro Limano 25: 161 (1973).
49. Webster. I. Asbestos and malignancy. S. Afr. Med. J. 47: 165 (1973).
50. Greenberg. M.. Lloyd Davies, T. A. Mesothelioma register 1967-68. Brit. J. Ind. Med. 31: 91 (1974).
51. Hain. F... Dalquen. P., and Bohlig, H. Katamnestische untersuchungcn zur Genese des Mesotheliomas. Inf. Arch. Arbeitsmed. 33: 15 (1974).
52. Nurminen, M. The epidemiologic relationship between pleural mesothelioma and asbestos exposure, Scand. J. Work Environ. Health I: 128 (19751.
53. Sturm, W. Bcricht uher die. X. mesothelium Konferenz. Wien. 7. Ges. Hyg. 21: 254 (1975).
54. Ziclhuis, P. I... Verstccg. J. P. J., Planteijdt, H. T. Pleural mesothelioma and exposure (o asbestos. Int. Arch. Occup. Environ. Health 36: 1.
55. McDonald. A. D., Magncr, D.. and Eyssen, G. Primary malignant mesothelial tumors in Canada, 1960-1968. A pathologic review by (he mesothelioma panel of the Cana dian Tumor Reference Centre. Cancer, 31; 869 (1973).
56. Newhouse. M., Berry. G., Wagner, J. C., and Turok, M. E. A study of the mortality of female asbestos workers. Brit. J. Ind. Med. 29: 134 (1972).
57. McCatighcy, W. T. E.. and Oldham. P. D. Diffuse mcsolhcljomas: morbid anatomical and histological diag nostic criteria including observer variation in histological diagnosis. In: Proceedings of the Conference on Biological KIVeets of Asbestos, P. Bogovski, J. C. Gilson, V. Timbreil. and J. C. Wagner, 1ARC, Lyon, 1973. p. 58.
58. Newhouse. M. L. Cancer among workers in the asbestos textile industry. In: Proceedings of the Conference on Biological Effects of Asbestos, P. Bogovski, J. C. Gilson, V. Timbreil. and J. C. Wagner, Eds., 1ARC, Lyon, 1973. p. 203.
59. Gilson. J. C. Asbestos cancer: past and future hazards. Proc. Roy. Soc. Med. 66: 395 (1973).
60. Hammond, E. C., and Selikoff. 1. J. Relation of cigarette smoking to risk of death of asbestos-associated disease among insulation workers in the United States. In: Pro ceedings of the Conference on Biological Effects of Asbes tos. P. Bogovski. J. C. Gilson. V. Timbreil, and J. C. Wagner, Eds.. IARC, Lyon, 1973, p. 312.
61. Newhouse. M. I... and Berry, G. The risk of developing mesothelial tumors among workers in an asbestos textile factory. Paper piesented at the XVIII International Con gress on Occupational Health. Brighton. England, Sept. 14-19. 1975.
62. Weill, 1L, Hughes. J., and Waggenspack. C. Influence of dose and liber type on respiratory malignancy risk in asbes tos cement manufacturing. Am. Rev. Resp. Dis. 120: 345 (1979).
63. Deny, (!.. Gilson, J. Holmes. S., I.ewinsohn, H. C. and Roach, S. A. Asbestosis: a study of dose-response relation ships in an asbestos textile factory. Brit. J. Ind. Med. 36: 98 11979).
64. Baselga Monte. M.. and Scgarra. F. Epidemiologic study of asbestosis in the Barcelona area: a'dose-response relation ship. I'apei piesented at the XIX International Congress on
dives February 1980
9
Occupational Health. Dubrovnik. Yugoslavia, September
25-.10. 1978. 65. l;o\. A J.. and ('oilier. P. I:. low mortality rates in iiuluv
trial cohort studies due to selection lot wotk and survival in the industry. Hi it. J. Prcv. Soc. Med. 1(1: 225 (1976).
66. Entcrline, P . DeCoulle. I'., and Henderson. V. Mortality in
relation to occupational exposure in the asbestos industry. J
Occup. Med. 14. 897 (19721. 67. Ilorow, M., Conston. A.. I.iverncsc. I... anil Sehalet. N.
Mesothelioma following exposure to asbestos: a review of 72 cases. Chest 64: 641 (1971).
68. Wagner. J. C. Diffuse pleural mesothelioma and asbestos
exposure in the Northwestern Cape Province. Ilrit. J. Ind. Med. 17: 260 (I960). 69. Harrington. J. S.. Gilson. J. C., and Wagner. J. C. Asbestos and mesothelioma in man. Nature 212: 54 (1971). 70. Wehster. I. Malignant pleural mesothelioma in an asbestos worker. Med. J. Austral. 49: 952 (1971). 71. McNulty. J. C. Malignant pleural mesothelioma in an as bestos worker. S. Air. Med J. 47: 165 (1962). 72. Jones. J. F. P.. I'ooley. P. D.. and Smith. P. (i. Paetory populations exposed to crocidolite asbestos: a continuing
survey. In: Environmental Pollution and Carcinogen Risk (INERM Symp. Ser.. Vol. 52). IARC. l.yon, 1976. p. 117 71. McDonald. A. D.. and McDonald, J. C. Mesothelioma attci
crocidolite exposure during gas mask manufacturing. Envi ron. Res. 17: 140.(1978). 74. McDonald. J. C\. Becklake. M. R.. Gibbs. G. W.. Mc Donald. A. D., and Rossiter. C. E. The health of chrysolite asbestos mine and mill workers of Quebec. Arch. Environ. Health 28: 61 (1974). 75. McDonald. J. C. Exposure relationships and malignant mesothelioma. In: Proceedings of Asbestos Symposium. Johannesburg, South Africa, .1-7 October 1977, H. W. Glen. Ed. National Institute for Metallurgy. Randhurg. 1977. 76. Kogan, E. M., Cmselnikova, N. A., and Gulevskaya. M. R. The cancer mortality rale among workers in the asbestos industry of the Urals. Gig. Sunil. 17: 29 (1972). 77. Selikoff, 1. J. ClinicaEsuryey of chrysotile asbestos miners and millers in Baire Verte. Newfoundland -- 1976. Report to the National Institute of Environmental Health Sciences. December 22, 1977. 78. Rossiter, C. E., Bristol. I . J., Cartier, P. II., Gilson. J C.. Grainger. T. R., Sluis-Ciemer. (i. K.. and McDonald. J. C. Radiographic changes in chrysotile asbestos mine and mill workers in Quebec. Arch. Environ. Health 24: 188 (1972). 79. Robinson. C. F., I emen. R. A., and Wagoner. J. K. Mortal ity patterns. 1940-1975. among workers employed in an as bestos textile IVictiffn and packing products manufactuiing facility. In: Dusts and Disease. R. A. l.emen, and J. M. Dement, Eds., Pathotox Publishers. Park Forest. III. 1979. 80. Mancuso, T. F. and E.l Attar. A. A. Mortality pattern in a cohort of asbestos workers. A study based on employ ment experience J. Occup. Med. 9 147 (1967). 81. Weiss, W. Mortality of a cohort exposed to chrysotile as bestos. J. Occup. Med. 19; 7)7 (1977). 82. Acheson. F.. D.. and Gardner. M. J. Mesothelioma and exposure to mixtures of chrysolite and amphibole asbestos. Arch, of Environ. Health. IX): 240 (1979). 81. Selikoff. 1. J.. Hammond. E. C , and Chute, J. Cat cinogenicity of amostle asbestos. Arch, luiviron. Health 25: 181(1972). 84. Seidman. II.. l.ilis, R.. anil Selikoff, I. J. Short-term asbes tos exposure and delayed cancer risk In: Proceedings of Thitd Intctuational Symposium on Detection and Preven tion of Cancer. Pan I. Vol. I. H. E Niching, lid.. Marcel Dekker. New York. 1976. 941 960. 85. Scidinan. H.. Selikoll. I. J.. and Hammond. Ei. C. Short-
tc.im asbestos woik exposures and long-term observadv
Ann N Y. Acad. Sci.. 110: 61 (1979).
86. NIOSII (1972): Criteria for a lccotnmcmled standout Occupational (exposure to Asbestos, U.S. Department'
HEW. Public Health Service. 1ISM 72-10267.
^
87. Johnson. W. M.. l.emen. R. A., and Hurst. G. A Re'P-"
tiny morbidity among workers in a plant manutacUin'
antosite insulation. In preparation.
_
88. Murphy. P. 1 . H.. Ciaeusler. E. A.. Ferris. B. G.. Fit/ger>
M.. Sallaiday. N.. and Morrisey. W. Diagnosis of ".i'N*
losis". Observations from a longitudinal survey ol shipw'
pipe covercrs. Am. J. Med. 65: 488 (1978).
89. Gillum. J. D.. Dement. J. M.. I emen, R. A.. Wagoner. J. K
Archer. V. E., and Blcjer. H. P. Mortality patterns anu'1
hard rock gold miners exposed to an ashestiform miners
Ann. N Y. Acad. Sci. 271: 145 (19761.
uo. McDonald. J. C.. Gibbs. G. W.. Liddell. F. V. D..
McDonald. A. D. Mortality after long exposure to cits'
mingtonite grunerilc. Am. Rev. Resp. Dis. 118 271 (19'Si 91. Mem man. 1... Kiviluoto. R.. and Haicama. M. Mortahtv ab
morbidity among the working population of anlhophyll'5
asbestos miners in Finland. Brit. J. Ind. Med. II: 105 (tuTh
92. Kiviluoto. R. Pleural calcification as a roentgenologic sign**
nonoccupational endemic anlhophyllite-asbestosis. Ac*
Radiol. (Snppl) 195: I 11960).
i
91. Meunna'n, I.. Asbestos bodies and pleural plaques in a Fit
nish series of autopsy cases. Acta Pathol. Microbiol. Scald
(Snppl ) 181: I (1966).
94. Selikoll'. 1. J. Epidemiology of gastrointestinal cancer. Em*
ron. Health. Perspect. 9: 299 (1974).
95. Schneidemian. M. A. Digestive system cancer among pef
sons subjected to occupational inhalation of asbestos part' cles: a literature review with emphasis on dose respond
Environ. Health Perspect. 9: 107 (1974).
96. Slell. P. M., and McGill. T. Asbestos and laryngeal car
cinoma. l ancet 2: 416(1971).
97. Shedigara. P. T.. and Morgan. R. W. Asbestos, smokingan>
laryngeal carcinoma. Arch. Environ. Health 10: 517 (19751
98. Newhouse. M. I... and Berry. G. Asbestos and larynge*
carcinoma, l ancet 2: 615 (1971). 99. Anderson, H. A.. l.ilis. R.. Daum. S.. Fischbein. A., aid
Selikoff. 1. J. Household exposure to asbestos and risk cl
subsequent disease. In: Dust and Disease. R. A. 1 .emen. aid
J. M. Dement. Eds.. Pathotox Publishers. Park Forest. Ill-
1979.
100. Wagner. J. C., Sleggs. C. A., and Marchand, P. Difftnt
pleural mesothelioma and asbestos exposure in the North
Western Cape Province. Brit. J. Ind. Med. 17: 260 (19601
101. Bolilig. II. and Haiti. E. (1977): Cancer in relation to eD
vironmental exposure, type of fibre, dose, occupation aid
duration of exposure. In: Proceedings of the Conference i't
Biological Effects of Asbestos. P. Bogovski, J. C. GiNon-
V. Timhicll. and J. C. Wagner, lids.. IARC. l.yon. 197.1
p. 217.
.
'
102 Gilson. J. C. Asbestos health hazards. Recent observation1 in the United Kingdom. In: Pneumoconiosis. Proceedingsd
the International Conference. Johannesburg. H. A. Shapiri).
Eil.. Oxlbtd University Press. 1970. p 171.
ItD. Doll. R. The age distribution of cancer: Implications for
models of carcinogenesis. J. Roy. Statist. Soc. AIM: 111
(1971)
'
104. Betty. (I . Newhouse. M. 1... and Turok. M. Combined
effects of asbestos exposure and smoking on mortality front
lung cancer in factory woikers. l ancet 2: 476 1 1972).
105. I emen. R. A. Lung cancer in female asbestos workers
Letter to Vernon Rose. Director. Division of Criteria IXveumcntation and Standuids Development. 1976.
106 Hammond. E. C.. Selikoff. 1. J.. and Seidman. H. Asbe'U*
10 Knvirotiim'ittal Health Perspective*
. observation. I |
exposure, cigarette smokirie and death rales Ann. N.V. Acad. Sci.. 331): 473 (1979).
standard . I j(|7 Liddell. F. I). K.. McDonald. J C.. and I'homas. I). C
icpai intent of j I
" Methods of cohort analysis: appiaisal hy application to as heslos mining. J. Roy. Statist Soc. AI41): 4fi9 (1977).
; A Respira. | jog Qridhord, K., Dccoullc. IV. I innmeni. J I .. Hocl. I). (I..
iMinifiicturing
../il/gcrald, I is of "ashes. E
y of shipyard 1
'goner. J. K., terns among irm mineral.
V D.. and ure to cum : 271 (1978). .lonality and mthophyllite : 105(1974). ulogic sign of stosis. Acta
lues in a Finubiol. Scand.
:ancer. Envj. ig per-
t-s partise response.
iryngeal car-
. smoking and l: 517(1975). md laryngeal
>ein. A., and s and risk of . I.emen. and s Forest. Ill
I. P Diffuse n the North . 2f><) <l%0). lution to encupation and onference on
Gilson,
f . 1973, observations roceedings of . A. Shapiro,
ilications for c. A 134: 133
t. Combined lortalily Ironp
(1972). los woikers. t of Criteria 1976.
II Asbestos
'iTxpectives fthruary 1 *>80
Hoover. R. N.. Rail. I). P.. S.dlioti. LI.. Schneiderman. M. A., and t 'pton. A C. Estimates of the fraction of cancer in the Cnited States related to occupational factors. National Cancer Institute. National Institute of Environmental Health Sciences, National Institute for Occupational Safety and Health. September 15. 1978. p. 39.
I