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OCR for page 3412
Proc. Natl. Acad. Sci. USA
Vol. 96, pp. 3412-3419, March 1999
Colloquium Paper
This paper was presented at the National Academy of Sciences colloquium "Geology, Mineralogy, and Human Welfare, "
held November 8-9, 1998 at the Arnold and Mabel Beckman Center in Irvine, CA.
A risk assessment for exposure to grunerite asbestos (amosite) in
an iron ore mine
R. P. NOLAN*T, A. M. LANGER*, AND RICHARD WILSON!
*Environmental Sciences Laboratory, Brooklyn College of The City University of New York, 2900 Bedford Avenue, Brooklyn, NY 11210;
and i:Harvard University, 9 Oxford Street Rear, Cambridge, MA 02138
ABSTRACT The potential for health risks to humans
exposed to the asbestos minerals continues to be a public
health concern. Although the production and use of the
commercial amphibole asbestos minerals grunerite (amos-
ite) and riebeckite (crocidolite) have been almost completely
eliminated from world commerce, special opportunities for
potentially significant exposures remain. Commercially viable
deposits of grunerite asbestos are very rare, but it can occur
as a gangue mineral in a limited part of a mine otherwise
thought asbestos-free. This report describes such a situation,
in which a very localized seam of grunerite asbestos was
identified in an iron ore mine. The geological occurrence of the
seam in the ore body is described, as well as the mineralogical
character of the grunerite asbestos. The most relevant epide-
miological studies of workers exposed to grunerite asbestos
are used to gauge the hazards associated with the inhalation
of this fibrous mineral. Both analytical transmission electron
microscopy and phase-contrast optical microscopy were used
to quantify the fibers present in the air during mining in the
area with outcroppings of grunerite asbestos. Analytical
transmission electron microscopy and continuous-scan x-ray
diffraction were used to determine the type of asbestos fiber
present. Knowing the level of the miner's exposures, we
carried out a risk assessment by using a model developed for
the Environmental Protection Agency.
We evaluate the potential for any risk to health in miners that
might arise after the release of grunerite asbestos from a seam
in an iron ore mine. None of the analytical criteria required for
the mineral's identification were ambiguous (the objects stud-
ied were asbestos fibers, not cleavage fragments). A geological
survey of the asbestos seam indicated localization in a rela-
tively small area of the mine. No asbestos of any other variety
was detected in the blast pattern and drill core samples. To
evaluate the potential for asbestos exposure, an air sampling
program that included area and personal samples was initiated.
Both types of samples were analyzed by phase-contrast optical
microscopy and analytical transmission electron microscopy
(ATEM). The risk assessment calculations were referenced to
the fibers >5 ,um long, with fiber counts obtained by phase-
contrast optical microscopy using standard National Institute
of Occupational Safety and Health-Mine Safety and Health
Administration (MSHA) methods.
The grunerite asbestos identified in the iron ore mine is a
known human carcinogen and merits special attention, al-
though its presence in the mine appears to be an anomaly. The
best evidence for the pathogenicity of grunerite asbestos has
come from epidemiological studies of workers in factories
where predominantly this fiber type was used. The mortality
studies of lung cancer, mesothelioma, and asbestosis among
grunerite asbestos exposed workers are reviewed.
PNAS is available online at www.pnas.org.
In addition, lung content analysis using ATEM was used to
characterize the fiber concentrations found in lung tissues of
individuals who developed asbestos-related diseases after ex-
posure. The results of the air sampling program are used to
calculate the mine work required to inhale a similar number of
fibers as that found in the lungs of mesothelioma cases.
The exposures measured in the iron ore mine are several
factors of ten lower than the occupational exposures that
occurred in the studied groups. Unlike the comparisons of lung
content described above that assumes a threshold, the Envi-
ronmental Protection Agency (EPA) model assumes a linear
dose-response, where each exposure is associated with an
incremental increase in risk.
Brief Review of the Occupational Health Effects Associated
with Asbestos Exposure. The earliest reports on the health
effects of exposure to asbestos occurred among individuals
who were exposed predominately to chrysotile asbestos (1~.
The first case in the English literature of asbestos-related
nulmonarv fibrosis described as asbestosis was reported in
1927 and occurred in a chrysotile textile worker. Although the
first medical indications of any effect of asbestos on health was
reported in 1906 in France and the United Kingdom, it (as with
other diseases, like silicosis) was frequently complicated by the
presence of tuberculosis. However, by 1938, asbestosis was
generally accepted by industry and government health units as
an occupational disease with distinct clinical, radiological, lung
function, and pathological characteristics.
Case reports of lung cancer accompanying asbestosis first
began to appear in the literature during the 1930s. The
evidence associating these diseases was greatly strengthened by
the information Merewether provided for the 1947 Report of
the Chief Inspector of Factories (England). He reviewed the
accumulated data from 1923-1946 and found a 13.2% preva-
lence of lung cancer among the 235 autopsies of individuals
know to have died with asbestosis, compared with 1.3% in
6,884 cases of silicosis. A high prevalence of lung cancer was
found among other autopsy series of asbestosis cases, such as
Wyer (1949), where 14.8% lung cancer was found among 115
asbestosis deaths (1), although at a meeting in Zagreb in 1953,
Merewether (2) expressed doubt about the relationship be-
tween asbestosis and cancer of the lung, perhaps because of the
limitations of an autopsy series.
In 1955, Sir Richard Doll published a comprehensive epi-
demiological survey of employees of chrysotile asbestos textile
plant in Rochdale, England (3~. Individuals employed for 20 or
more years experienced lung cancer ~14 times more fre-
quently than the general population (11 cases observed/0.8
expected). The results became available at the same time that
Abbreviations: ATEM, transmission electron microscopy; SMR, stan-
dardized mortality ratio; OSHA, Occupational Safety and Health
Administration; MSHA, Mine Safety and Health Administration.
iTo whom reprint requests should be addressed. e-mail: rnolan@
brooklyn.cuny.edu.
3412
OCR for page 3413
Colloquium Paper: Nolan et al.
the association between lung cancer and cigarette smoking was
being established. Defining the increase in the risk of devel-
oping lung cancer when an individual's exposure to chrysotile
asbestos is insufficient to produce asbestosis is mostly theo-
retical. Changes in the diagnostic criteria of asbestosis have
further complicated the matter.
In 1960, Wagner et al. (4) reported 33 cases of a malignant
tumor known as mesothelioma, which he attributed to cro-
cidolite exposure. The discovery focused attention on the
question of asbestos fiber type and disease. This rare tumor was
the last of the three major asbestos-related diseases to be
identified. The potency of chrysotile to induce this tumor in
humans remains a subject of considerable controversy. It also
is clear that exposure to crocidolite asbestos, actinolite-
tremolite asbestos, and grunerite asbestos produce consider-
ably higher incidence of this disease, sometimes even after
exposures that are considered quite low. The patterns of
mesothelioma depending on asbestos fiber type are strikingly
different in that a high mortality for mesothelioma is never
found among individuals exposed only to chrysotile asbestos
(5), although from time to time, individuals present with
pleural mesothelioma and high concentrations of chrysotile
are found to be present in the pulmonary tissue by lung content
analysis (64.
Geological Survey of the Area of the Mine Containing
Grunerite Asbestos. The grunerite asbestos is confined to
quartz-ankerite-grunerite veins of the host rock. These veins
contain medium- to coarse-grained quartz, ankerite, stilpno-
melane, and grunerite fiber distributed throughout a specific
bench face (Fig. 1~. The veins range up to 3 feet thick. The
major veins occur within a magnetite-chart-silicate unit at the
contact of the host rock and metadiabase sill units. The larger
veins generally conform to the compositional banding of the
host rock, but smaller veins commonly cut across the structure.
Long-fibered asbestos mineral development is restricted to the
thicker conformable veins.
Grunerite asbestos is developed within the quartz-ankerite-
stilpnomelane veins and along its contact with the host rock
and sills. The veins were deformed structurally, exhibiting signs
of shearing, brecciation, faulting, and folding. Minor quartz-
carbonate veins occur, which lack asbestos-like minerals.
The grunerite asbestos is discontinuous along the strike of
the veins. Locally, recrystallization or replacement within the
host rock has resulted in relatively coarse-grained acicular
Proc. Natl. Acad. Sc'. USA 96 (1999J 3413
amphibole. The coarse-grained amphiboles are most notable
in the silicate layers, but occur occasionally within the mag-
netite-chert bands, particularly near grunerite asbestos. Fi-
brous amphiboles occur irregularly in cross-cutting and con-
cordant vein-like structures over a gradational zone from the
host wall rock, with fairly coarser "rained amphiboles, to
quartz-ankerite-stilpnomelane-grunerite veins. The coarse
grunerite asbestos occurs discretely within, and immediately
adjacent to, the quartz-ankerite-stilpnomelane veins (Fig. 2~.
Strongly sheared horizons in the host rock close to the veins
have formed platy, bladed, and fibrous mineral habits, only
some of which are asbestiform. At several places along the
strike of the quartz-ankerite-stilpnomelane-grunerite veins,
the host rock has been tightly folded immediately adjacent to
the vein (several inches on both sides). Essentially no defor-
mation is observed just inches away from tight folding.
Banded, vuggy, quartz-fluorite-pyrite-chalcopyrite veins
occur locally (most notably at the extreme southern end of the
mapped bench) possibly in association with the quartz-
ankerite-stilpnomelane-grunerite veins. The mineralogy and
appearance of the sulfide veins indicate a different generation
of development, but no clear cross-cutting relationships were
observed. Minor quartz-magnetite-pyrite-chalcopyrite veins
and veinlets occur.
Analysis of Bulk Samples. Three bulk samples, selected
from highly fibrous seams, were analyzed by polarized light
microscopy, continuous-scan x-ray diffraction, and ATEM. In
the United States, MSHA and the Occupational Safety and
Health Administration (OSHA) regulate six minerals under
the asbestos standard (Table 1~. Five are amphiboles. These
minerals have diverse elemental compositions (7~. Each of the
named minerals can exist in three different morphological
forms or habits (8) that have been shown to effect their
biological potential (9~. In the asbestos habit, the fiber occurs
as parallel fibrils, which form polyfilamentous bundles. It is this
habit that is believed to cause cancer, and only this asbestos
habit is regulated by MSHA and OSHA. The two other habits
are nonasbestiform, occurring as splintery fiber, and massive
anhedral nodules. When crushed, however, the nonasbesti-
form amphiboles may form elongated cleavage fragments that
morphologically resemble fibers. Difficulties arise when cleav-
age fragments occur in association with amphibole asbestos.
Two of the asbestos minerals (cummigtonite-grunerite and
tremolite-actinolite) form a solid solution series in which Fez+
FIG. 1. The grunerite asbestos occurred along the wall and on top of the lower bench on the left.
OCR for page 3414
3414 Colloquium Paper: Nolan et al.
FIG. 2. The coarse grunerite asbestos vein occur within, and
immediately adjacent to the quartz-ankerite-stilpnomelane veins.
and Mg2+ substitute. Although actinolite, grunerite, and
tremolite do occur in nature as asbestos minerals, an occur-
rence of cummingtonite asbestos has not been reported.
All three of the highly fibrous samples were analyzed by
polarized light microscopy, continuous-scan x-ray diffraction,
and ATEM. None of the analytical criteria required for the
mineral's identification are ambiguous (10~. The asbestos seam
is localized to a relatively small area of the mine. No other
asbestos fiber type was detected in 24 blast pattern and drill
core samples collected to evaluate the depth to which the seam
extends.
Evaluation of Air Samples from the Mine. To evaluate the
potential for asbestos exposure by inhalation, an air sampling
program (including both area and personal samples) was
initiated. The personal samples were job classification-specific
and sufficient in number to evaluate the range of exposures
that would occur during mining of the ore. Of the 179 personal
air samples collected, the mean concentration was 0.05 fiber
per ml (all fiber-5 am), and the highest exposure was 0.39
fiber per ml (all fiber-5 Em) (Table 2~. None exceeded the
MSHA asbestos standard (2 fiber per ml) (all fiber-5 Am) or
action level, although 13.4% did exceed the current OSHA
asbestos standard of 0.1 fiber per ml (all fiber-5 Am) (Table 3~.
Comparison of Epidemiological Studies of Workers Ex-
posed to Iron Ore Dust and Those Exposed to Asbestos Dust.
The four epidemiological studies described cover mortality.
Such studies of causes of death,are used to determine whether
a cohort (a group of individuals defined by exposure to some
agent) dies more frequently from a particular disease than
would otherwise be expected (based on rates in the reference
population, e.g., everyone in the U.S.A.~. Diseases such as lung
cancer occur with a natural background. Cigarette smoking
elevates the expected background death rate, and cancer
Table 1. Mineralogy of the six minerals regulated under the
occasionally referred to as cummingtonite-grunerite asbestos
Commercial name
Amosite
Anthophyllite asbestos
Chrysotile
Crocidolite
Tremolite asbestos
Actinolite asbestos
Proc. Natl. Acad. Sci. USA 96 (1999J
Table 2. Results of the analysis of three hundred and twenty-s~x
air samples collected while mining a grunerite asbestos (amosite)
seen by the NIOSH-7400 methods
No. of
Air sample samples
Area
During mining
During blasting
Total
Personal
Drilling
Shovel
Production truck
Track dozer
Blast
Unidentified Sample
Total
Total samples analyzed
Field
Laboratory
Unspecified
Not analyzed
Total samples taken
TValues given as arithmetic mean + SD the fiber concentrations a
log normal.
"Controls, values are fibers per mm2 of filter area.
Concentration of
fibers per mll
(all fibers 25
Em in the air)
137 0.02 + 0.02
10 0.01 + 0.01
147
110 0.06 + 0.05
22 0.06 + 0.09
23 0.04 + 0.05
20 0.05 + 0.04
2 0.03 + 0.03
2 0.05 + 0.03
179 0.05 + 0.05
326 0.04 + 0.05
11 5.2!
7 2.71
2 1.61
3
349
Range of fiber
concentration
0.001-0.20
0.002-0.02
0.001-0.23
0.008-0.39
0.005-0.24
0.005-0.17
0.013-<0.05
0.028-0.07
0.001-0.39
0.001-0.39
incidence may be further increased by exposure to certain
environmental agents. The assumption is made that the frac-
tion of people that smoke is the same in the exposed as the
control group. Epidemiological cohort studies allow for the
determination of association between exposure to some agent
and an increase in the occurrence of a specific disease. The
standardized mortality ratio (SMR) is the number of deaths
observed of a specific disease in the cohort divided by the
number of deaths from that cause expected for the reference
population, multiplied by 100. As the years of exposure
increases, the SMR should also rise because of the increase in
dose.
A cohort of 17,800 asbestos insulation workers in the United
States and Canada was followed from January 1, 1967 until the
end of 1986 (11, 12~. At the end of 1986, after almost 302,000
person-years of observation, 4,951 deaths occurred, while only
3,453 deaths were expected. The increased incidence of lung
cancer accounted for >50% of the excess deaths (Table 4~. The
SMR (100 x observed/expected cases) for lung cancer was
435, whereas 8.6% and 9.3% of the deaths were caused by
asbestosis and mesothelioma, respectively. Although the insu-
lators were exposed to all of the commercial asbestos fiber
types, the major fiber type retained in the worker's lung tissue
was grunerite asbestos (12~.
, asbestos standard in the United States. Amosite is
Mineral name
Grunerite
Anthophyllite*
Chrysotile
Riebeckite
Tremolite*!
Actinolite*!
Mineral group Chemical formula
.
(Fe2+, Mg)7[sisO22] (OH)2t
(Mg, Fe2+)7[sis°22] (OH)2
Mg3[Si20s] (OH)4
Na2Fe3+2(Fe2+, Mg)3[Si8022] (OH)2
Ca2Mas[SisO22] (OH)2
Ca2(Mg, Fe2+)s[SisO22] (OH)2
Amphibole
Amphibole
Serpentine
Amphibole
Amphibole
Amphibole
*These minerals do not have separate names for their asbestos analogs. Mineralogists now refer to amosite as grunerite asbestos
and cocidolite as riebeckite asbestos, although the commercial names persist in the literature.
TTremolite-actinolite also form a solid-solution series between a calcium-magnesium-end member (tremolite) and a
calcium-iron magnesium-end member (actinolite).
TFor amositc (gruncrite asbestos) the Fez+ is present in at least 5 of the 7 available x structural sites.
OCR for page 3415
Colloquium Paper: Nolan et al.
Table 3. United States regulations concerning occupational
exposure to asbestos fiber
2.0
0.2
0.1
Regulatory
agency
MSHA
OSHA*
oSHAt
Standard for an
8-hour
time-weighted
average, asbestos
fibers per ml
Excursion
level, fibers
per ml
=10t
None Allowed
None Allowed
All data refer to all fibers-5 ,um.
*Department of Labor Reg. 1986, 29CFR 1910-1926. Effective July 21,
1986.
TDepartment of Labor Reg. 1994, 29CFR 1910, Effective October 11,
1994.
tIn a 15-min period.
Action level,
asbestos
fibers per ml
1.0
0.1
0.05
Vermiculite Ore Containing Tremolite Asbestos. The min-
eral vermiculite has the generalized chemical formula (Mg,
Ca)0.35(Mg, Fe, Al)3(Al, Si)4O~o(OH)2nH2O. On heating, the
mineral loses water rapidly and expands to form a lightweight
aggregate used for various purposes, e.g., insulation, soil
conditioning, and filter medium. Various amphibole minerals
associated with vermiculite have been the focus of health
concerns, rather than vermiculite itself.
The health effects among the miners and millers in Libby,
Montana exposed to vermiculite containing tremolite asbestos
have been studied by two groups of investigators (13-17~. Each
investigation was designed as a mortality study and a cross-
sectional chest radiographic survey. Slightly different criteria
were used to define each cohort: the McDonald study (13, 14)
contained 406 men with 165 deaths, and the Amandus study
(15-17) contained 575 men with 161 deaths. Both research
groups used historical air samples to estimate exposure indices
for the cohort members. The dust levels in the past were made
with a device called a midget impinger, and the unit of
concentration of dust was expressed in millions of particles per
cubic foot (mppcf) of air. Conversion factors have been used
to change the mppcf unit to an approximate number of fibers
per milliliter of air (fibers per ml-5 lam), the units used in
modern risk assessment (13, 15, 18~.
The exposure in the mill before the installation of dust
control equipment in 1964, was estimated to be 400 and 168
fibers per ml (all fiber -5 lam), respectively. Dust levels
between 1965 and the closure of the mill in 1974 were
estimated by McDonald et al. and Amandus et al. to ~20 and
~33 fibers per ml (all fiber-5 am), respectively. These were
the highest exposures measured except for 20% higher dust
levels during floor sweeping.
McDonald and colleagues calculated the SMR for total
mortality as 117, with 23 lung cancers observed against 9.4
Proc. Natl. Acad. Sci. USA 96 (1999J 3415
expected (SMR = 245) and 4 mesotheliomas (2.4%~. The
SMR for the total mortality in the Amandus cohort was 110,
with 20 lung cancers where ~9 cases were expected (SMR =
223) and 2 mesotheliomas (1.2%~. The lung cancer SMR for
>20 years since first exposure for all exposure levels were 242
and 279 for the McDonald and Amandus cohorts, respectively.
Both cohorts had an SMR of 250 for nonmalignant respiratory
disease.
Two Cohort of Minnesota Iron Ore Workers. Taconite is a
term used particularly in the Lake Superior region of Minne-
sota for certain iron-containing rocks from the Biwabik Iron
Formation. A high-grade ore concentrate is obtained from
commercial-grade taconite that contains enough magnetite
(Fe3O4) to be economically processed by fine grinding and
wet-magnetic separation. Taconite is a hard, dense, fine-
grained metamorphic rock that contains substantial quartz
(20-50%) and magnetite (10-36%) and various mineral con-
stituents, including hematite, carbonates, amphiboles (princi-
pally of the cummingtonite-grunerite series, although actin-
olite and hornblende also occur), greenalite, chamosite, min-
nesotaite, and stilpnomelane.
Reserve Mining Company. Analysis of mortality data ob-
tained on men who were employed from 1952-1976 has been
reported (194. The study was initiated by concerns in the early
1970s that asbestos was released into the air and dumped into
lake water during processing of the taconite rock (20, 21~. It
was inferred that this dust posed a risk to the miners as well as
to the general public. Silver Bay and Duluth obtained their
drinking water from Lake Superior, into which the pulverized
waste rock (or tailings) from the pellet plant was deposited at
Silver Bay. The U.S. Department of Justice considered this a
Potential health hazard. The Department alleged that the
amphibole in the waste rock (cummingtonite-grunerite) was
asbestos and the exposures would cause gastrointestinal cancer
through ingestion and lung cancer from inhalation of the
water- and airborne fibers (although they had done no calcu-
lation of this).
The Reserve cohort consisted of 5,751 men, of which 907
had worked for the company for >20 years and 298 were
deceased. The men had been exposed to respirable dust
concentrations from 0.02 to 2.75 mg/M3, the modal range
being 0.2-0.6 mg/M3. The fibrous particulate content of the
dust was occasionally >0.5 fibers per ml (all fibers 25 ,u m), but
usually the concentration was much lower.
The observed and expected deaths and SMR for all men who
had worked one year or longer from 1952-1975 are given in
Table 5. There was no relationship between the mortality
observed and lifetime exposure to silica dust (that was as high
as 1,000 mg/M3 x years). There was no suggestion that deaths
from cancer increased after 10 or 20 years of latency. No
deaths from mesothelioma or asbestosis were reported.
Table 4. Deaths from lung cancer asbestosis and mesothelioma* among 17,800 asbestos insulation workers in the United States and
Canada (1967-1986~*
Asbestosis
Mesothelioma
Years from onset Lung Cancer SMRNo. per No. per
of exposure Person-years E O O/E O 100,000 per yr O 100,000 per yr
-
<15 61,655 3.9 9 2321 1.6 0 0
15-19 52,709 11.637 318 14 26.6 5 9.5
20-24 57,595 27.595 346 31 53.8 18 31.8
25-29 50,518 46.6183 393 52 102.9 73 144.5
30-34 37,165 57.4281 490 59 158.8 105 287.5
35-39 20,340 46.8239 511 84 413.0 91 447.4
40-44 10,200 30.8155 503 80 784.3 59 578.5
45-49 5,256 18.875 399 33 627.8 58 1103.4
>50 6,151 25.494 370 73 1,186.8 49 796.6
Total 301,593 268.71168 435 427 141.6 458 151.9
*Best evidence: Causes of death categorized after review of best available information (autopsy, surgical, and clinical). E' expected; O.' observed.
OCR for page 3416
3416 Colloquium Paper: Nolan et al.
Proc. Natl. Acad. Sci. USA 96 (1999
Table 5. Selected causes of mortality for men who worked one year or longer for the Reserve Mining Company
Deaths
Cause of death ICD* Expected Observed SMR
All causes 000-E999 343.7 298 87
Cardiovascular disease 402, 404, 410-429 123.8 112 90
Cancers
All 140-209 63.4 58 92
Respiratory 160-163 17.9 15 84
Digestive 150-159 17.6 20 114
Urinary 188-189 3.0 3 101
Genital 180-187 3.3 3 91
Selected nonmalignant respiratory diseases 470-474, 480-486, 490, 6.8 4 59
491, 493, 510-519.
All external causes E800-E998 72.8 76 104
Motor vehicle accidents ES10-ES23 31.2 38 122
Source: Higgins et al. (1983)
*International Classification of Causes of Death, 8th Revision.
"Standardized mortality ratio, based on white male mortality in Minnesota, 1952-1976.
Minnesota Taconite Miners. A second epidemiological
study of Minnesota taconite workers employed at the Erie and
Minntac mines was reported (22~. The study cohort, followed
from 1947-1988 with a minimum observation period of 30
years for all participants, was made up of 3,341 men, of which
1,058 were deceased. Dusts in the two mines are reported as
containing 28-40% and 20% quartz at Erie and Minntac mine,
respectively. Concentrations of fibrous particulates were
nearly always <2 fibers per ml (all fibers ~5 lam). These
fibrous particulates included elongate cleavage fragments and
are assumed to be similar to those objects reported at Reserve
Mining. The total number of deaths was significantly fewer
than expected, SMR = 83 (based on U.S. male rates) and 91
(based on Minnesota male rates). SMR for all cancer (includ-
ing lung cancer), diseases of the circulatory system, and
nonmalignant respiratory disease were fewer than expected
when compared with both reference groups (Table 6~.
There was one reported case of mesothelioma in a 62-year-
old worker whose exposure to taconite had begun only 11 years
before his death. Although latency periods as short as 15 years
have been reported among insulation workers, mesothelioma
generally occurs following a long latency period of 25 years or
more (23~. This person had previously been employed in the
railroad industry, as a locomotive fireman and engineer, an
occupational environment where both amosite and crocidolite
asbestos insulation was used and opportunity for exposure
existed (12~. It is unlikely that this particular taconite exposure
contributed to the appearance of mesothelioma.
Analysis of the mortality data, with a minimum latency
period of 30 years, provided no evidence to support any
association between exposure to quartz or elongated cleavage
fragments of amphibole with lung cancer, nonmalignant re-
spiratory disease, or any other specific disease.
Comparison of Occupational Cohorts Exposed to Iron Ore
and Asbestos. The American and Canadian asbestos insulation
workers are generally thought to have had exposure to the
three principal commercial asbestos fiber types grunerite
asbestos, crocidolite, and chrysotile (12~. The tremolite asbes-
tos in the vermiculite at Libby, Montana has never been
extensively used in commerce in the United States. The
vermiculite workers are an example of the effect of amphibole
asbestos at concentrations of ~1% in the ore. The mortality
experience of the two asbestos-exposed groups are distinctly
similar. Each shows an elevated risk of lung cancer, mesothe-
lioma, and asbestosis (a nonmalignant respiratory disease). Of
the 1,058 deaths reported in the most recent study of Minne-
sota taconite workers, one would have expected about 250 lung
cancer (23.6%) and about 98 mesotheliomas (9.3%) if their
mortality experience was similar to American and Canadian
insulators (114. Instead, the actual number of lung cancer and
mesotheliomas (Table 6) was 65 (6.1%) and 1 (0.09%), re-
spectively.
Actually 32 fewer lung cancer occurred than the 97 expected
(SMR = 67) using the rates for U.S. white males. The one
mesothelioma that did occur had a latency of ~11 years in
taconite mining. In the large insulation cohort (17,800 work-
ers), no mesothelioma was reported with a latency <15 years,
indicating the present case was unlikely to be related to his
taconite dust exposure (11, 23~. The mortality experience of
the iron ore workers is, in fact, overall less than expected,
indicating they are healthier than the general population. This
healthy workers effect is commonly observed among many
employed groups.
Epidemiological and Lung Content Analysis of Grunerite
Asbestos-Exposed Workers. Before the United States entering
Table 6. Deaths by major causes (1948-1988) in taconite miners
and millers exposed for 3 months or more before 1959
Cause of death
(ICD, 7th Revision, 1955)
All causes (001-998)
All malignant neoplasms (140-205)
Digestive organs and peritoneum
(150-159)
Stomach (151)
Large intestine (153)
Deaths
Expected Observed SMR
1,272.5
267.7
Respiratory system (160-164)
Bronchus, tracheas, lung
(162-163)
Kidney (180)
Lymphopoietic (200-205)
All diseases of circulatory system
(400-468)
Arteriosclerotic heart disease (420)
Cirrhosis of liver (581)
Nonmalignant respiratory disease
(470-527)
All external causes of death (800-998)
All accidents (800-962)
Motor vehicle accidents (810-835)
Suicide (963, 970-979)
Cause unknown
Number of workers
Number of person-years
Deaths per 1,000 person-years
Adjustment of cause-specific SMRs for
missing Certificates
1,058
232
70.5
12.0
23.9
97.0
92.2
6.8
25.8
83
87
66 94
11 92
26 109
65 67
62 67
12 177
29 112
575.1 477 83
481.8 368 76
35.5 24 68
77.2
112.3
74.4
33.4
27.3
55 71
114 102
79 106
32 96
32 117
19
3,431
10,055
10.5
+1.8%
Source: Cooper et al. (22)
OCR for page 3417
Colloquium Paper: Nolan et al.
Table 7. Fiber count (given in millions of fibers per gram of dried
lung tissue) by type of pathology
Pathology
Lung Cancer
Mesothelioma
Other
Mean
SD
Grunerite
Asbestos
Total (Amosite)
Mean
Number
SD of Cases
14
s
24
1,483
1,035
358
2,568 1,433
1,039
490
1,000
297
2,590
1,013
463
Source: Gibbs et al. (254.
World War II, a grunerite asbestos factory was established in
Paterson, New Jersey to supply the U.S. Navy with asbestos
insulation for the pipes, boilers, and turbines in ships. From
1941-1945, 933 men were recruited to work in this plant, which
operated until November 1954. Of these, 820 men formed a
cohort and provided a unique group of individuals with an
intense short-term exposure and a long-term follow-up (244.
Among these individuals, no mesotheliomas occurred with
less than a 6-month exposure history or a latency of <20 years.
Although the concentration of asbestos fibers in the air of the
Paterson plant was never determined, few occupational health
experts would estimate the exposure at <30 fibers per ml (all
fibers-5 lam). Therefore, 6 months of work at the plant is
equivalent to 15 fibers per ml x years. The mean fiber levels
in the iron ore mine are 0.05 fibers per ml. Therefore, it would
require about 300 years of exposure in the iron ore mine to
reach the 15 fiber per ml x years level.
For the workers in the Paterson plant the concentration of
grunerite asbestos present in the lung tissue of any individual
with an asbestos-related disease has not been reported. How-
ever, in a report about workers in a British grunerite asbestos
factory, lung tissue taken at autopsy from 14 lung cancer and
5 mesothelioma cases were examined for fiber levels (25~. The
mineral fibers were separated from the lung tissue and ana-
lyzed by using ATEM. Although the factory principally used
grunerite asbestos, a small amount of chrysotile had also been
used. Of the 43 cases in which sufficient tissue was available for
fiber analysis, grunerite asbestos was present at a 20-fold
higher concentration than the three other commercial asbestos
fiber types. In both the lung cancer and mesothelioma cases,
~97% of the total fiber burden was grunerite asbestos (Table
7~. The mean fiber concentration was about 1.483 x 109 and
1.035 x 109 fibers per gram of dry lung tissue for lung cancer
and mesothelioma, respectively. The mean fiber concentration
was ~45~o higher in the lung cancer cases than in the me-
sothelioma cases.
Assuming the total dry weight of an average pair of human
lungs to be ~150 am, the mean total concentration of fiber in
the five mesothelioma cases would be 1.5 x 10~i fibers (25~.
The mean fiber concentration in the air of the iron mine was
0.05 fibers per ml (all fibers ~ brim). The fiber number in the
lung tissue represents fibers of all lengths, whereas the air data
is only for those-5 ,um. The 0.05 fibers per ml (all fibers >5
Am) represents an index of the fibers present in the air.
The fibers <5 ,um and-5 ,um but too thin to be visible by
phase-contrast microscopy were not counted. One method to
approximate the total number of fibers per ml is to interpolate
from data where the total size distribution of grunerite asbes-
tos has been reported, as at the Penge Mine in the Republic
of South Africa (26~. Using the length and diameter data from
Penge and assuming 0.05 fibers per ml represents the fibers ^5
,um in lengths and-0.25 ,um in diameter, a multiplication
factory of 6.2 was interpolated. The total fiber concentration
in the iron mine is therefore assumed to be 0.05 fibers per ml x
6.2, or 0.33 fibers per ml (all fibers). A second method is to add
the fiber counts of 11 air samples from the mine analyzed by
phase-contrast optical microscopy and ATEM to estimate total
Proc. Natl. Acad. Sci. USA 96 (1999) 3417
exposure. When the two values were added, the mean exposure
was 1.18 + 0.57 fibers per ml (all fibers). The exposure is
3.6-fold greater than that estimated by using the size distribu-
tion of grunerite asbestos in the Penge mining environment,
although the mean exposure for the 11 air samples was 0.08 +
0.05 fibers per ml (all fibers ~5 lam), which exceeds the average
of the 179 personal air samples of 0.05 + 0.05 fibers per ml (all
fibers >5 ,um). All of the grunerite asbestos fibers counted by
ATEM were <5 ,um long.
To inhale a concentration of fibers similar to the concen-
tration in the lung tissue of the mesothelioma cases (1.5 x 10~i
fibers) would require inhaling 4.7 x 10~i ml of air in the iron
ore mine, assuming an exposure of 0.33 fibers per ml. For the
purpose of this model, we pessimistically assume no clearance,
although the lung has mechanisms to clear inhaled particles
that can be very effective. Assuming on average an individual
inhales 10,000 ml of air per minute, this is 600,000 ml per hour,
or 4,800,000 ml per 8-hour shift. This seems a very large
number, but it would require ~98,000 days in the iron ore mine
with an exposure of 0.33 fibers per ml (at 1.18 fibers per ml
exposure, it would require 27,000 days) just to inhale a similar
number of fibers to that found in the only series of lung content
analysis of grunerite asbestos-related mesotheliomas. The
range is 75-265 years of daily 8-hour shifts of exposure to
Table 8. Risk of death in a lifetime for some selected
environmental exposures
Activity
Lifetime risk
per 100,000
Heavy cigarette smoking
All causes of death
Lung cancer only
Total
U.S. motor vehicle accidents
All deaths
Pedestrian deaths
U.S. air pollution (calculated deaths from assumed
correlation)
Frequent airline passenger, 200,000 miles for 35
years
Accident
Cosmic ray cancers
U.S. natural radiation background at sea level
(cancers) excluding radon gas
U.S. home deaths
All
Falls (mostly over age 65)
Drowning deaths (nontransport causes)
Diagnostic x-ray in USA (cancer)
Person living with a smoker (cancer)
Person in brick building, added natural radiation
One transcontinental round-trip flight per year
Accident
Cosmic rays
Upper level of risk EPA claims to regulate
Falling meteorite
Drinking water with 100 mg/ml choloroform (EPA
level)
Eating 1.1 kg charcoal-broiled steak per week
(cancer only)
World Health Organization (1974) acceptable risk
for drinking water
Struck by falling airplane (average over entire U.S.~*
Smoking three cigarettes in a lifetime (all deaths)*
Lower level of risk EPA claims to regulate*
Lightning*
35,000
9,000
23,000
1,200
100
2,000
400
300
200
600
200
80
200
100
70
15
15
15
s
2
0.4
0.3
0.1
0.1-0.15
*Those activities with lifetime similar to the lung cancer and mesothe-
lioma risk calculated for the iron ore miners. All other activities listed
pose a higher risk.
OCR for page 3418
3418 Colloquium Paper: Nolan et al.
Proc. Natl. Acad. Sc'. USA 96 (1999)
Table 9. Lifetime risk for 1-year continuous exposure per 100,000 people for 0.001 fibers per ml
Age on onset
of exposure Average*
Lung Cancer Risk
Nonsmoker Smoker
0.31 0.06 0.62
Total Cancer Risk
Mesothelioma Risk Nonsmoker Smoker
0.83
0.6
0.53
30
45
50
0.21
0.25 0.05 0.50
0.03
0.27
0.1
0.08
*From Table 6-3 EPA (1986) for men.
inhale a similar number of fibers to that found in the lung tissue
of the factory mesothelioma cases.
Risk Assessment from Mining in the Iron Ore Mine. In the
past, workers were exposed to aerosols containing high con-
centrations of asbestos fibers. To obtain a quantitative risk
estimate from the low exposures, we used a model developed
for the Environmental Protection Agency to quantify the risk
of asbestos-related disease (27~. This model is developed to fit
the type of data described above, the exposures during mining
of the iron ore are orders of magnitude lower than the
occupational exposures which occurred in the cohorts used to
parameterize the dose component in the equations of the risk
models. Nonetheless, the high exposure-response relationships
of the past were used to interpolate the risk to the current low
exposures encountered in the iron ore mine in linear (propor-
tional) relationships. We know of no scientist who has argued
that this linear dose-response model underestimates the risk.
The risk assessment model requires that the concentrations of
asbestos fibers in the air be determined. Risk assessment is
based on counting all fibers ~5 ,um in length in the occupa-
tional environment by phase-contrast microscopy, at ~ x500
magnification (Table 2~.
Risk estimates were considered for the following two sce-
narios: (i) A bench containing approximately 1 million tons of
rock was removed in 22 days. Assuming the average employee
is 45 years old, what is the lifetime risk for lung cancer and
mesothelioma? No air sampling was done at that site, and it is
uncertain whether any asbestos exposure took place. Assume
the fiber levels are similar to those given in Table 2. (ii)
Approximately 30 days of drilling remain to be done on the
bench containing the seam of grunerite asbestos (28 days in the
sill and two days in the waste iron formation). Assuming the
sill contains no asbestos (so far none has been found), what
would be the lifetime risk to the drillers for lung cancer and
mesothelioma assuming they are 45 years old?
Table 6-3 from the EPA risk model (27) was used. This table
is for an exposure to a concentration over a long time. It can
be used for a 2- or 22-day exposure if it is assumed that the
exposure integrated over time is the relevant parameter. (i)
There is a linear dose-response relationship. Any proposed
biological mechanism of which we are aware involves the
exposure integrated over time. (ii) If the peak exposure is the
parameter of concern, the risk is proportional to the frequency
of peak exposures. The integrated exposure is also propor-
tional to the total time of possible exposure and goes down
with time.
The average lung cancer risk among smokers and nonsmok-
ers was reported by the EPA. The risk number found in the
EPA Table 6-3 is the average for smokers and nonsmokers, but
the actual lung cancer risk from asbestos exposure is five times
less for nonsmokers and double for smokers. Because me-
sotheliomas are assumed not to be related to smoking, the
number applies to both smokers and nonsmokers.
Exposure. The average of the exposures monitored is ap-
propriate for calculating the risk to a worker not otherwise
identified. The mean airborne concentration of 179 personal
air samples was O.OS fibers per ml (all fibers >5 Am) (Table 2~.
This value assumes all the fibers were asbestos and that each
person was continuously exposed (8-hour time-weighted av-
erage) over a 22-day period. The EPA calculated for contin
uous exposure over different periods of time, and therefore the
iron ore mining exposure is converted to be equal to the
exposure average over 1 year, . = 22/365 x 8/24 x
0.05 = 0.01 fibers per ml (all fibers-S ~m). The life-time risk
can be read directly from Table 6-3 (27) at 30 and SO years of
age at onset of exposure (45 years of age is interpolated)
(Table 9~.
Scenario I. The total cancer risk for the individual expo-
sure beginning at 45 years of age is 0.1 and 0.6 in lOO,OOO for
nonsmokers and smokers, respectively (see Table 8 for
comparison with selected different lifestyles and environ-
mental exposures). This assumes a linear dose-response. If
all of the cancer risk is assumed to be lung cancer, it is
equivalent to smoking 2 or 12 cigarettes in a lifetime for 0.1
and 0.6 in 100,000 people respectively. The risk for someone
smoking one cigarette is 0.05 per 100,000 people (or, smok-
ing 2 cigarettes is associated with a lung cancer risk of 1 in
1 million).
Scenario II. In this scenario, there will be a 2-day exposure
(not the 22-day of Scenario I), so the risk becomes 2/22 or 1/11
of the risk of Scenario I (0.1 in 1,000,000 for nonsmokers, and
0.6 in 1,000,000 for smokers) (Table 10~.
These are risks accumulated in a lifetime. Note also that
according to the assumption pertaining to the risk calculation;
each new exposure adds to this risk independent of the past
risk. Of course, if asbestosis is a precondition for lung cancer,
there exists a lung cancer threshold (28, 29~. Although new
exposures can add to past ones, they only increase the risk
where the total exposure exceeds the threshold. That the EPA
model overestimates the risk of lung cancer is widely believed
(30~. Although the above is a best estimate, an important
consideration is how much larger could the risk be to that
individual. An examination of Table 2 indicates the extreme
exposure level of 0.39 fibers per ml (all fibers ~5 Am) was
seven times larger than the mean O.OS fibers per ml (all fibers
-5 lam). This suggests the most extreme risk is seven times
greater than given above. These risks are put into perspective
in Table 8.
We thank Mr. Paul Nordstrom for providing the survey of the bench
containing grunerite (amosite) asbestos. We acknowledge support
from a Higher Education Advanced Technology grant from the State
of New York and Cleveland-Cliffs, Inc.
Table 10. Lifetime risk for two mining scenarios in the iron ore
mine compared to selected relative risks*
Activity
Lifetime risk
per lOO,000
Iron Ore Mining
Scenario I
Nonsmokers
Smokers
Scenario II
Nonsmokers
Smokers
Lung cancer heavy cigarette smoking
US motor vehicles, all deaths
Drowning deaths, nontransport caused
Upper limit of risk EPA claims to regulate
*See Table 8 for additional comparison.
0.1
0.6
0.01
0.06
9,000
1,200
80
15
OCR for page 3419
Colloquium Paper: Nolan et al.
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Representative terms from entire chapter:
lung cancer
