WORKPLACE EXPOSURE TO ASBESTOS 

Review and Recommendations 

DHHS (NIOSH) Publication No.81-103 

NIOSH-OSHA 

Asbestos Work Group 

April 1980 

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES . Public Health Service 

Center,s for Disease Control 

National Institute for Occupational Safety and Health 

U.S. DEPARTMENT OF LABOR 

Occupational Safety and Health Administration 

November 1980 

For sale by the Superintendent of Documents , U.S . Government 

Printing Office, Washington, D.C . 20402 

CONTENTS 

PAGE 

MEMORANDUM ON ASBESTOS UPDATE 

AND RECOMMENDED OCCUPATIONAL 

STANDARD 1 

I. ASBESTOS NOMENCLATURE/DEFINITIONS 9 

Review 9 

General Definition 10 

II. ASBESTOS SAMPLING AND ANALYSIS 12 

III. BIOLOGIC EFFECTS OF EXPOSURE TO 

ASBESTOS IN ANIMALS 14 

In Vivo 14 

In Vitro 16 

IV. BIOLOGIC EFFECTS OF EXPOSURE TO 

ASBESTOS IN HUMANS 16 

Arnosite 16 

Chrysotile 18 

Crocidolite 20 

Mixed Fiber Types 21 

Malignant Neoplasms other than Mesotheliorna 

and Cancer of the Lung 24 

V. SMOKING AND ASBESTOS 25 

VI. EXPOSURE TO ASBESTIFORM MINERALS 

OTHER THAN COMMERCIALLY MINED 

ASBESTOS 28 

VII. NON-OCCUPATIONAL EXPOSURE TO 

COMMERCIAL SOURCES OF ASBESTOS 30 

VIII. DOSE-RESPONSE RELATIONSHIPS 30 

REFERENCES 33 

111 

MEMORANDUM FOR: Dr. Eula Bingham 

FROM: 

SUBJECT: 

Assistant Secretary for 

Occupational Safety and Health 

Dr. Anthony Robbins 

Director, National Institute for 

Occupational Safety and Health 

Asbestos Work Group 

The Updated Scientific 

Information on Asbestos and 

Recommended Occupational 

Standard for Asbestos Exposure 

In the fall of 1979, a NIOSH/OSHA committee was formed 

at the direction of Dr. Eula Bingham, Assistant Secretary of 

Labor for Occupational Safety and Health, and Dr. Anthony 

Robbins, Director of the National Institute for Occupational 

Safety and. Health (NIOSH), to review the scientific information concerning asbestos-related disease and assess the adequacy of the current OSHA occupational health standard of 

2,000,000 fibers per cubic meter greater than 5 μmin length 

(2Mf/m3). Since the 1972 promulgation of this 2,000,000 f/m3 

standard, OSHA, in 1975, proposed lowering the standard to 

500,000 f/m3

; NIOSH, in 1976, recommended lowering the standard to 100,000 f/m3

; and the British Advisory Committee on 

Asbestos, in 1979, recommended lowering its occupational exposure standards. The NIOSH/OSHA committee has reviewed 

the most recent scientific information, including documents 

concerning the above developments and the 1977 International 

Agency for Research on Cancer (IARC) review of the carcinogenicity hazards of asbestos, and presents the following major 

conclusions and recommendations. A detailed updating of significant scientific literature since the 1976 NIOSH Criteria 

Document and the 1977 IARC Monograph is attached. 

1 
1. Definition of Asbestos. Having considered the many factors 

involved in specifying which substances should be regulated as 

asbestos, the committee recommends the following definition: 

Asbestos is defined to be chrysotile, crocidoli te, and fibrous cummingtonite-grunerite including amosite, fibrous tremolite, 

fibrous actinolite, and fibrous anthophyllite. The fibrosity of the above minerals is 

ascertained on a microscopic level with fibers defined to be particles with an aspect 

ratio of 3 to 1 or larger. 

2. Sampling and Analysis of Airborne Asbestos. The committee 

concludes that the membrane filter-phase contrast microscopy 

method represents the only technique available that can reasonably be used for routine monitoring of occupational exposures and sampling for compliance purposes. However, the 

committee recognizes the lack of specificity of this method for 

fiber identification, and recommends the use of supplementary 

methods such as electron microscopy for fiber identification in 

cases of mixed fiber exposures. In recommending the primary 

use of light mi~roscopy, the committee also wants to stress the 

inability of this method to detect short asbestos fibers to which 

workers are exposed. The toxicity of asbestos fibers shorter 

than the 5-micrometer detection limit of light microscopy cannot be dismissed on the basis of current scientific information. 

3. Biologic Effects of Exposure to Asbestos. Animal studies 

demonstrate that all commercial forms and several noncommercial forms of asbestos produce pulmonary fibrosis, 

mesothelioma, and lung neoplasms. Chrysotile is as likely as 

crocidolite and other amphiboles to induce mesotheliomas after 

intrapleural injection, and also as likely to induce lung neoplasms after inhalation exposures. 

Human occupational exposures to all commercial asbestos 

fiber types, both individually and in various combinations, 

have been associated with high rates of asbestosis, lung cancer, 

and mesothelioma. While significant excesses of cancer of 

several other sites have been observed in exposed workers, 

presently available information is insufficient to determine the 

role of specific fiber types. 

On the basis of available information, the committee concludes that there is no scientific basis for differentiating between asbesto_s fiber types for regulatory purposes. Accordingly, 

the committee recommends that a single occupational health 

standard be established and applied to all asbestos fiber types. 

2 
Available data show that the lower the exposure, the lower 

the risk of developing asbestosis and cancer. Excessive cancer 

risks, however, have been demonstrated at all fiber concentrations studied to date. Evaluation of all available human data 

provides no evidence for a threshold or for a "safe" level of 

asbestos exposure. Accordingly, the committee recommends 

that, to the extent uses of asbestos cannot be eliminated or less 

toxic materials substituted for asbestos, worker exposures to 

asbestos must be controlled to the maximum extent possible. 

4. Inadequacy of Current 2,000,000-Fiber Occupational Standard. The committee concluded that a variety of factors demonstrates that the current 2,000,000-fiber standard is grossly inadequate to protect American workers from asbestos-related 

disease. First, the 2,000,000-fiber standard was designed in 

1969 by the British Occupational Hygiene Society (BOHS) for 

the limited purpose of minimizing asbestosis. Disease prevalence data from the BOHS study population collected subsequent to 1969 strongly suggest that this standard is insufficient 

to prevent a large incidence of asbestosis. Second, all levels of 

asbestos exposure studied to date have demonstrated asbestosrelated disease, and a linear relationship appears to best describe the shape of the dose-response curve. These considerations led the committee to conclude that there is no level of 

exposure below which clinical effects do not occur. Third, the 

absence of a threshold is further indicated by the dramatic 

evidence of asbestos-related disease in members of asbestosworker households and in persons living near asbestos-contaminated areas. These household and community contacts 

involved low level and/or intermittent casual exposure to asl;>estos. Studies of duration of exposure suggest that even at 

very short exposure periods (1 day to 3 months) significant 

disease can occur. 

Although various models can be and have been fashioned 

to postulate possible dose-response relationships involving asbestos, the committee believes that thelimited current data 

preclude the creation of any one empirical curve to describe the 

exact dose-response relationship. Over the last three decades, 

measurement techniques for asbestos have changed in several 

crucial respects, and there have been no suitable methods available to date to compare the results of prior techniques to current 

methods. 

3 
In addition, no adequate epidemiological information is 

available on the disease experience of workers exposed below 

the current standard and followed for a sufficient period to 

identify long latent effects. Consequently, the committee cannot present a precise dose-response relationship for the variety 

of asbestos-related diseases. However, the committee firmly believes that compelling evidence demonstrates that prevention 

of asbestos-related diseases requires that an occupational standard minimize all asbestos exposures, and definitely be set far 

below the current 2,000,000-fiber standard. 

5. Recommended Occupational Standard for Asbestos Exposure. Given the inadequacy of the current 2,000,000-fiber standard, the committee urges that a new occupational standard be 

promulgated which is designed to eliminate non-essential asbestos exposures, and which requires the substitution of less 

hazardous and suitable alternatives where they exist. Where 

asbestos exposures cannot be eliminated, they must be controlled to the lowest level possible. A significant consideration 

in establishing a permissible exposure limit should be the lowest level of exposure detectable using currently available analytical techniques. At present this level would be 100,000 fibers 

greater than 5 μm in length per cubic meter averaged over an 

8-hour workday. Regardless of the choice of a permissible exposure limit, the best engineering controls and work practices 

should be instituted, and protective clothing and hygiene facilities should be provided and their use required of all workers 

exposed to asbestos. Respirators are not a suitable substitute 

for these control measures. The committee also reiterates its 

judgment that even where exposure is controlled to levels below 

100,000 fibers, there is no scientific basis for concluding that all 

asbestos-related cancers would be prevented. 

6. Medical Surveillance Program. Appropriate medical surveillance is crucial to detect and minimize the progression of some 

asbestos-related diseases. Considerable emphasis should be 

placed on baseline medical examinations for all workers potentially exposed or who have been exposed to asbestos at any 

level. These examinations should include the following: (1) a 

14" x 17" postero-anterior chest X-ray; (2) spirometry including 

forced vital capacity (FVC) and forced expiratory volume in one 

second (FEV 1 ); (3) a physical examination of the chest including auscultation for the presence or absence of rales, rhonchi, 

4 
and wheezing; (4) an assessment of the presence or absence of 

finger clubbing; and (5) a history of respiratory symptoms and 

conditions including tobacco smoking. 

An occupational history should include a history of exposure to asbestos and exposure to other substances of real or 

potential medical significance. Performance criteria for these 

procedures, including the periodicity of subsequent medical 

surveillance, should be developed by NIOSH in consultation 

with OSHA and professional societies and organizations concerned with the diagnosis and prevention of respiratory diseases. The committee does not recommend comprehensive annual medical examinations as presently required. Sputum cytology should be evaluated in the development of an improved 

medical surveillance program. The committee believes that 

sputum cytology may prove to be a valuable supplement to 

X-ray evaluation. 

It is also crucial that all required medical surveillance be 

promptly evaluated and the results reported to the employee. 

Furthermore, the standard should provide for periodic reporting of aggregate medical information concerning an employer's 

entire workforce. Results at a minimum should be displayed in 

a non-identifiable, aggregate format so that the employer, employees, and OSHA can see the prevalence of abnormalities 

possibly associated with asbestos-related disease, and also see 

how this prevalence has changed over time. 

The committee recognizes that OSHA's recent lead standard contains a multiple physician review mechanism whereby 

workers can get independent medical evaluations by physicians 

of their choice. The lead standard also contains a medical removal protection program whereby workers can obtain special 

health protection where necessary, accompanied by appropriate 

economic protection. The committee feels that these programs 

are relevant to asbestos workers and should be considered as 

part of a new occupational asbestos standard. 

Medical records generated due to the standard's medical 

surveillance program should be maintained for at least 40 years 

or for 20 years after termination of employment, whichever is 

longer. 

7. Other Recommendations. The committee further r_ecommends the following: (1) Due to the widespread current and past 

uses of asbestos products in the maritime and construction in5 
dustries, it is vital that any new asbestos standard address 

these industry sectors as well as other workplaces with employees exposed to asbestos. Regulation of these industries should 

be structured around the principle that where work must be 

done using asbestos, only those employees needed to do this 

work should be present, and only for the minimum period of 

time needed to complete this work. 

(2) Due to the sampling and analytical difficulties concerning asbestos, manufacturers of asbestos-containing products 

such as construction materials should perform detailed monitoring of exposures which could result from all foreseeable uses 

of their products, including misuse. This monitoring should 

include electron microscopy to identify fiber type mix and exposures to fibers less than 5 μ,min length. This monitoring data 

should accompany these products downstream so the users not 

only know that asbestos exposures may occur, but also know 

the nature of potential exposures. This monitoring data could, 

if appropriate, avoid the need for small employers who use 

asbestos-containing products to have to conduct monitoring on 

their own. 

(3) Due to the fact that other agencies regulate occupational exposu:::es to asbestos (such as the Mine Safety and 

Health Administration), these agencies should be urged to 

participate in the development of a new standard and adopt 

this new standard. 

(4) Because cigarette smoking enhances the carcinogenic 

effect of asbestos exposure on the lung, particular emphasis 

should be placed on this in any educational program developed 

under a new standard. 

6 
Richard A. Lemen, M.S. 

Chairman of the OSHA/ 

NIOSH Asbestos Work 

Group 

Assistant Chief 

Industry Wide Studies 

Branch 

NIOSH 

David H. Groth, M.D. 

Chief 

Pathology Section 

Division of Biological 

and Behavioral Sciences 

NIOSH 

John M. Dement, M.S. 

Deputy Director 

Division of Respiratory 

Disease Studies, NIOSH 

J. William Lloyd, Sc. D. 

Senior Epidemiologist 

OSHA 

Han K. Kang, Dr. P.H. 

Health Scientist 

OSHA 

Robert L. Jennings, Jr., J.D. 

Special Assistant to the 

Assistant Secretary 

OSHA 

Joseph K. Wagoner, S. D. Hyg. 

Senior Epidemiologist 

NIOSH 

7 

I. ASBESTOS NOMENCLATURE/DEFINITIONS. 

Review 

There is considerable controversy as to which mineral particles should be considered "asbestos" insofar as demonstrated 

health effects are concerned (Campbell et al., 1977; Ampian, 

1978; Zoltai, 1978; Langer, 1979). Until recently, most environmental and epidemiological studies concerning mineral fibers 

were focused on occupational cohorts exposed to asbestos fibers 

from commercial deposits. However, there is currently much 

interest in exposures to other minerals such as submicroscopic 

amphibole fibers and cleavage fragments and related health 

effects. Mineralogists have voiced concern that mineralogical 

terms have been used improperly, potentially classifying many 

non-asbestos materials as asbestos (Ampian, 1978; Campbell et 

al., 1977; Zoltai, 1978). 

An important problem which exists is the basic definition 

of what minerals should be called "asbestos." Various definitions have been proposed or used: 

National Academy of Sciences (1977): 

"The name for a group of naturally occurring hydrated silicate minerals possessing fibrous morphology and commercial 

utility." 

Bureau of Mines (1977): 

"(l) A collective mineralogical term encompassing the asbestiform varieties of various minerals; (2) an industrial product 

obtained by mining and processing asbestiform minerals." Asbestiform minerals were further defined to be "a specific type of 

mineral fibrosity in which the fibers and fibrils possess high 

tensile strength and flexibility." 

!ARC (1977): 

"Asbestos is the generic name used for a group of naturally 

occurring mineral silicate fibers of the serpentine and amphibole series." 

Zoltai (1978): 

" ... a collective term referring to the unusual crystallization of 

certain minerals in the form oflong, strong, and flexible fibers, 

aggregated in parallel or radiating bundles from which fibers 

can easily be separated." 

9 
The above definitions demonstrate an important problem. 

That is, the condition of fibers in nature as a result of crystal 

growth is the only criteria for distinguishing asbestos from 

other silicates (Langer, 1979). Most properties mentioned above 

can only be measured on bulk samples (megascopic properties). 

However, airborne fibers in the occupational setting are only 

observable on the microscopic level, thus not allowing measurements of such properties as tensile strength and flexibility. 

Langer et al. (1979) have pointed out that, using strict mineralogical nomenclature, isolated submicroscopic single fibers derived from · known asbestos sources could not be termed 

"asbestos." In fact, among the many minerals demonstrating 

a fibrous habit in nature, only six minerals are commercially 

exploited and thus considered "asbestos." These include 

the serpentine mineral chrysotile and the amphiboles 

cummingtonite-grunerite including amosite, anthophyllite asbestos, tremolite asbestos, actinolite asbestos, and crocidolite. 

In addition to problems relative to exposures to mineral 

fibers other than one of the six mentioned above, acicular cleavage fragments are frequently indistinguishable from mineral 

fibers derived from commercial asbestos sources, especially on 

the submicroscopic scale. Cleavage plays an important role during commutation for some amphibole minerals. Submicroscopic 

amphibole mineral fragments often demonstrate structural 

and chemical properties indistinguishable from asbestos homologues. Airborne size characteristics such as length and diameter are often similar to asbestos. 

General Definition 

The foregoing considerations present a fundamental question of how broad a new or revised regulation should be. Arguments can be made for inclusion of all fibrous minerals posing 

risks comparable to commercially exploited fibrous minerals 

called asbestos. On the other hand, the fibrous minerals generally called asbestos appear to form the most pressing hazards 

to the largest number of current workers. This effort has not 

attempted to recommend coverage of all fibrous minerals or 

analogs, but has focused on commercial materials generally 

considered asbestos and asbestiform contaminants common to 

commercially exploited materials. We recommended the following definition for regulatory purposes, pending thorough and 

complete regulation of the hazards of all fibrous materials. 

10 
1. Asbestos is defined to be chrysotile, crocidolite, and fibrous 

cummingtonite-grunerite including amosite, fibrous temolite, 

fibrous actinolite, and fibrous anthophyllite. 

2. The fibrosity of the above minerals is ascertained on a microscopic level with fibers defined to be particles with an aspect 

ratio of 3 to 1 or larger. 

We also expressly adopt the following approach articulated 

by the recent British Advisory Committee on Asbestos (Vol. 1, 

p. 11): Asbestos is a generic term for the fibrous 

forms of several mineral silicates. These 

occur naturally in seams or veins, generally between about 1 and 20 millimetres 

(mm) in width in many igneous or metamorphic rocks and belong to one of two 

large groups of rock-forming minerals: the 

serpentines and amphiboles. 

We recognize the mineralogical complexities associated with the definition and 

identification of asbestos and asbestos 

fibre, but for the purposes of this report 

we concentrate on the fibre types with 

which people are most likely to come into 

contact as a result of their use in industry. The serpentine group contains the type 

of asbestos known as chrysotile ('white asbestos'), which is the only asbestiform 

member of this group of minerals and 

by far the commonest and commercially 

the most important type of asbestos. The 

amphibole group contains crocidolite ('blue 

asbestos'), amosite ('brown asbestos'), 

anthophyllite, actinolite and tremolite. 

Amosite is an acronym for Asbestos Mines 

of South Africa and is mineralogically known as cummingtonite- grunerite 

asbestos. Tremolite may occur as a contaminant with chrysotile and with other minerals such as talc. Crocidolite, amosite and 

anthophyllite have all been exploited commercially, although anthophyllite is no 

longer in significant quantities. 

The above definitions of asbestos should not be taken to 

mean that fibers or mineral fragments of other minerals are 

without biological significance (IARC, 1977). Although epidemiologic data for other "mineral fibers" are limited at this 

time, prudence dictates that such substances be handled with 

caution. 

11 
II. ASBESTOS SAMPLING AND ANALYSIS 

Update on New Methods 

Since the NIOSH revised recommended asbestos standard 

was published in December, 1976, there have been several new 

developments in the area of sampling and laboratory analysis. 

Kim et al. (1979) have developed a quick screening test for 

chrysotile, crocidolite, and amosite which can be used for bulk 

material samples. The test is based upon the formation of color 

complexes with Mg+2 and Fe+2 released from asbestos upon acid 

digestion. The Mg+2 from chrysotile is complexed with 

p-nitrobenzenazo-s-naphthol. The Fe+2 from crocidolite and 

amosite is complexed with 1,10-phenathroline. A positive test is 

indicated by formation of colored complex for Mg+2 and/or Fe+

2

• 

The test by Kim et al. is not specific for asbestos; however, the 

detection limit is reasonable for bulk samples with 1-2 mg being 

detectable in any given sample. Of 70 samples tested, 52 were 

correctly classified as containing asbestos or not, 18 samples 

gave false positives, and there were no false negatives. The 

method has little promise for airborne samples. 

Lange and Haartz (1979) have developed a method for 

chrysotile asbestos determinations by X-ray diffraction. The 

method for membrane filters involves ashing followed by redeposition on silver membrane filters. The 7.33A peak for 

chrysotile is primarily used in an integrated mode. Normalization using reflections from the silver membrane is employed 

along with X-ray absorption corrections. The lower limit of 

detection is reported to be 2 μg on a filter with good linear 

response to over 200 μg per filter. Minerals such as antigorite, 

lizardite, kaolinite, and possibly chlorite are potential interferences with chrysotile. The method has not been adapted for 

amphibole determinations. 

Lilienfeld and Elterman (1977) and Lilienfeld et al. (1979) 

have developed a portable monitor capable of real-time determinations of airborne fiber concentrations. The monitor is 

based upon rotation of elongated particles by means of a rotating electric field of large voltage gradient. Fibers of various 

lengths are then detected by synchronous detection of modulated light scattered from a continuous-wave helium-neon laser 

beam with modulation generated by the rotating particles. 

Concentrations between 0.001 and 30 fibers/cc are reported to 

be detectable. At a concentration of 1 fiber/cc, a relative stan12 
dard deviation of 10% is reported. The minimum detectable 

fiber length and diameter are estimated to be 2 μm and 0.2 μm, 

respectively. The instrument is not specific for asbestos as other elongated particles align within the electric field, and the 

instrument cannot be easily used for obtaining "breathing 

zone" samples. 

Gale and Timbrell (1979) have reported progress in development of an automated method for determining fiber density 

on membrane filters. The method involves first clearing the 

membrane filter by conventional methods followed by aligning 

fibers on the filter in a strong magnetic field. The sample is 

then placed in a specially designed microscope on a motor 

driven stage. Fiber density is determined by measuring light 

scattered from the rotating fibers. The method is not yet 

commercially available, but is predicted to have a lower 

limit of detection of about 0.1 fiber/cc based on a 4-hour sampling period. 

Optical Microscopy 

The phase contrast method recommended by NIOSH for 

compliance sampling in the occupational setting was reviewed 

in the 1976 NIOSH document. Since that review, Leidel et al. 

(1979) have reported studies to better define precision of the 

method at lower levels. Minor changes in fiber counting methods have also been recommended by NIOSH to correct a potential statistical bias. 

Based on the most recent data available, Leidel et al. (1979) 

estimated the coefficient of variation for the membrane filter 

sampling-phase contrast counting method to be 0.11 to 0.15, 

given a total count of at least 100 fibers. With a reduced fiber 

count of 10 fibers in the analysis, the coefficient of variation is 

estimated to be 0.41. Statistical tests based upon these estimates of precision are recommended by NIOSH for determining 

compliance or non-compliance with regulatory standards 

(Leidel et al., 1979). Procedures are available for single full 

shift samples, multiple samples covering the workshift, or short 

"grab samples." 

The phase contrast method is clearly capable of measuring 

airborne fiber levels down to 0.1 fibers/cc (fibers longer than 5 

μm) given that due consideration is given to inherently high 

variability at such levels. The method is highly sensitive for 

detection of fibers longer than 5 μm; however, specificity of the 

13 
method for identifying asbestos fibers may be a serious problem 

under certain circumstances. Fiber identification is based only 

upon fiber length and aspect ratio; therefore, the method is 

not specific in situations where a mixture of asbestos and nonasbestos fibers occur or where large numbers of other elongated 

particles are present. The lack of specificity becomes more serious at lower fiber concentrations, and alternate methods for 

identification are likely to be required. The most likely choice 

for fiber identification in airborne dust samples is electron microscopy where both electron diffraction and microchemical 

analyses may be used to identify fibers (NIOSH, 1976). The 

fraction of asbestos fibers determined by these methods could 

then be multiplied by phase contrast determinations to arrive 

at asbestos fiber levels. It seems reasonable that such determinations only need be made for a statistically determined 

sample and not for each airborne dust sample, with subsequent 

determinations made only upon process or product modifications. The statistical confidence of the airborne asbestos 

fraction determinations should be taken into account in determinations of compliance or non-compliance. 

In addition to the problem of lack of specificity for fiber 

identification, only a fraction of all airborne asbestos fibers are 

actually accounted for by the phase contrast method, which 

considers only fibers longer than 5 μm. The phase contrast 

method, therefore, can only be considered an "index" measure 

of fiber exposure. In fact, the fraction of airborne fibers longer 

than 5 μm is extremely variable, ranging from 1 to 50%, depending on fiber type and industrial operation (Dement et al., 

1976). In addition to determinations of fiber identification by 

electron microscopy, it may also be desirable to determine airborne fiber size and specifically the fraction of airborne fibers 

longer than 5 μm. 

III. BIOLOGIC EFFECTS OF EXPOSURE TO 

ASBESTOS IN ANIMALS 

In Vivo 

Animal studies reported since 1976, in which several types 

of asbestos have been utilized, further support the findings 

published in the NIOSH Revised Recommended Asbestos 

Standard. In that publication, reference was made to research 

which adequately demonstrated that all commercial forms and 

several other types of asbestos can produce mesotheliomas and 

primary bronchogenic neoplasms in animals. 

14 
Although mesotheliomas were most readily produced by 

intrapleural injections, they were also produced by inhalation 

exposures (Wagner et al., 1974). Since then, additional studies 

by Wagner et al. (1979) have shown that a commercial grade, 

predominantly short fiber Canadian chrysotile, which is used 

primarily for paint and plastic tile fillers, can induce mesotheliomas when injected intrapleurally into rats, and induce 

primary lung neoplasms when the animals are exposed by 

inhalation. 

Not only is chrysotile as potent as crocidolite and other 

amphiboles in inducing mesotheliomas after intrapleural injections (Wagner et al., 1973), but also equally potent in inducing 

pulmonary neoplasms after ~nhalation exposures (Wagner et 

al., 197 4). In terms of degree ofresponse related to the quantity 

of dust deposited and retained in the lungs of rats, chrysotile 

appears to be much more fibrogenic and carcinogenic than the 

amphiboles (Wagner et al., 1974). The concentration of dust in 

the lungs of rats exposed to Canadian chrysotile was only 

1.8-2.2% of the dust concentration in the lungs of animals exposed to amphiboles (after 24 months of inhalation exposures). 

Yet the lung tumor incidences and degrees of pulmonary fibrosis were similar in all groups. The reasons for higher incidences 

of lung cancer and mesotheliomas in workers exposed to amphiboles is, therefore, probably related to higher concentrations 

of respirable fibers during their exposures. 

Research to this day has not been able to establish a fiber 

length below which there exists no carcinogenic potential by 

inhalation, the most common route of occupational exposure. 

This is true because of the unavailability of specifically sized 

fibers (Pott, 1979). 

Not only were naturally occurring fibers carcinogenic, but 

synthetic fibers were carcinogenic as well. Pylev (1979) obtained mesotheliomas in 54% of rats injected intrapleurally 

with a milled synthetic hydroxy-amphibole, and primary lung 

neoplasms in 23% of hamsters injected intratracheally with a 

synthetic chrysotile. Mesotheliomas were also induced in 9/60 

hamsters injected intrapleurally with glass fibers, 82% of 

which were greater than 20 μmin length (Smith et al, 1979). 

Further experimentation with fibers of differing diameters 

and lengths supports the previous observation that long, thin 

fibers are much more carcinogenic than short or thick fibers. 

Utilizing 16 preparations of fiberglass of differing fiber lengths 

15 
and diameters, Stanton et al. (1977) were able to show that 

glass fibers with diameters less than 1.5 μm and lengths greater than 8 μm were carcinogenic in the pleura of rats, and that 

fibers shorter or wider than those were much less carcinogenic. 

For example, one preparation in which 60% of the fibers were 

less than 1.5 μm in diameter induced pleural sarcomas in 64% 

of rats, whereas another preparation in which only 16% of the 

fibers were less than 1.5 μm in diameter induced pleural sarcomas in only 14% ofrats. Ninety-five percent of the fibers in both 

preparations were greater than 8 μm in length. 

Besides the corroborating evidence for the carcinogenic 

potential of asbestos, recent results indicate a strong cocarcinogenic effect. Kung-Vosamae and Vinkmann (1979) reported a strong synergism between nitroso-diethylamine 

(NDEA) administered orally and chrysotile given intratracheally. NDEA given orally alone induced lung tumors in only 2% 

of the hamsters, whereas NDEA administered orally plus 

Canadian chrysotile given intratracheally induced lung neoplams in 40%. Chrysotile alone induced no lung tumors. 

Additional research on the transport of fibers into tissues 

has confirmed that fibers reach the lymphatics shortly after 

oral administration (Masse et al., 1979). In view of the ability 

of intratracheally administered chrysotile to act synergistically 

with at least one nitrosamine, it is possible that ingested 

asbestos could act synergistically with orally administered 

nitrosamines to induce cancer in the gastrointestinal tract. 

In Vitro 

In vitro studies of all commercial forms of asbestos have 

been inconsistent when repeated or performed at different laboratories. Their correlation with in vivo studies has also been 

inconsistent and, thus, their value in studying the etiology of 

asbestos induced diseases is unclear at present. 

IV. BIOLOGIC EFFECTS OF EXPOSURE TO 

ASBESTOS IN HUMANS 

Amosite 

Seidman et al. (1979) have extended their study of amosite 

asbestos workers with short-term exposures. The study group 

consisted of 820 men first employed between June, 1941 and 

December, 1945 in the production of asbestos insulation and 

16 
who were alive in 1961. Followup was through 1977, with expected deaths adjusted for age and calendar time estimated 

using death rates for white males in the general population of 

New Jersey. 

Among the cohort studied by Seidman et al., 83 lung 

cancers were observed according to death certificate information, whereas 23.1 were expected. Among 61 men employed less 

than 1 month, 3 lung cancers were observed versus 1.3 expected. Although based on small numbers, excess mortality from 

lung cancer showed an increasing trend with employment duration. Cancer latency periods were progressively shortened 

with increasing employment duration. Four mesotheliomas 

were reported on death certificates in contrast to 14 which were 

identified on autopsy and other tissue diagnoses. Three in the 

group had less than 1 year of exposure. Although no environmental data are available for this plant, dust counts were made 

in another plant using the same fiber type and production 

process. Seidman et al. reported average exposure at this plant 

to be 23 fibers/cc. Further data available for this comparison 

plant were published by NIOSH (1972) showing mean exposures to range from 14 to 75 fibers/cc. At such concentrations, 

a lung cancer relative risk of 2.3 could be calculated with employment less than 1 month. 

Anderson et al. (1979) evaluated the risks of non-malignant 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. Anderson et al. also reported a 35.9% prevalence 

of radiographic abnormalities among household contacts of 

former employees at this same amosite plant, compared with a 

4.6% prevalence among a control group. These radiographic 

abnormalities included pleural thickening, pleural calcification, pleural plagues, and irregular opacities. These studies 

raise the specter of non-occupational hazards associated with 

casual or low-level exposures to amosite. 

Murphy et al. (1978) reported a followup to their first report (1971) of shipyard pipe coverers exposed predominantly to 

amosite asbestos. Workers in the original Murphy report 

of 1971, with "asbestosis" diagnosed by multiple criteria, had a 

poor prognosis as reported in the 1978 longitudinal survey. 

17 
Chrysotile 

Robinson et al. (1979) reported an additional 8 years of 

observation and 385 deaths to the Wagoner et al. (1973) study 

of mortality patterns among workers at one facility manufacturing asbestos textile, friction, and packing products. Chrysotile 

constituted over 99% of the total quantity of asbestos processed 

per year, except for 3 years during World War IL During these 

3 years, amosite was selectively used to a limited extent because of U.S. Naval specifications, and accounted for approximately 5% of the total asbestos used per year. Crocidolite and 

amosite for the other years accounted for less than 1 % of total 

usage in very selected areas. Exposures to these other two types 

may have played some role in the etiology of disease; however, 

due to the overwhelming exposure of the cohort to chrysotile, it 

is likely that the other exposures played a minor role in the 

overall mortality patterns. Robinson et al. confirmed Wagoner 

et al.'s observations of statistically significantly excess deaths 

due to bronchogenic cancer, suicide, heart disease, and nonmalignant respiratory disease including asbestosis and a statistically non-significant excess of digestive cancer and lymphoma. Robinson et al. described 17 mesotheliomas whereas no 

mesotheliomas were detected in the Wagoner et al. study where 

observation of mortality ceased in 1967. The appearance of 17 

mesothelioma in the updated study reflects latency periods of 

24 to 53 years since onset of first exposure. Further analysis 

indicated 14 of 17 mesothelioma deaths occurred after the original study period. This observation confirms other findings that 

mesotheliomas are characterized by very long latency periods. 

Chovil and Stewart (1979) also reported latencies of 6 to 44 

years, with a mean of 26.9 years. 

Weiss (1977) reported no unusual mortality experience 

over a 30-year period for a cohort of workers employed in a 

paper and millboard plant stated to be using only chrysotile. 

The author concluded that the study results were suggestive of 

a minimal hazard from chrysotile. This conclusion must be 

viewed in light of the limitations inherent in the study. The 

study population was small (n = 264) and only 66 workers had 

died at the time of analyses. Two of these workers died of asbestosis. Moreover, the unusually low Standard Mortality Ratio 

(SMR) for many causes of death in the Weiss et al. paper suggests the possibility of a selection bias greater than that usually 

seen when rontrasting industrial populations with the general 

population. 

18 
McDonald et al. (1973, 1974) reported an increased risk of 

lung cancer among men employed in Quebec chrysotile mines 

and mills. The risk of lung cancer among those workers most 

heavily exposed was 5 times greater than those least exposed. 

Liddell et al. (1977) further analyzed the mortality experience 

of the cohort of chrysotile asbestos miners and millers previously studied by McDonald et al. and found excesses of respiratory cancer, asbestosis, and mesothelioma. These same 

chrysotile miners and millers of Quebec, as of 1977, had experienced nine confirmed and two suspected mesotheliomas 

(McDonald, 1978). The author concluded for the seven cases 

observed at Thetford mines that "There is therefore no good 

reason to doubt chrysotile exposures as the cause." 

A recent study by Nicholson et al. (1979) examined the 

mortality of 544 Quebec chrysotile mine and mill employees 

which corresponded closely in terms of duration of exposure and 

periods of observation to cohorts of mixed fiber asbestos factory 

workers and insulation workers established iri other studies. 

Among this cohort of 544 men with at least 20 years of employment in chrysotile mining and milling at Thetford Mines, Canada, 16% of the deaths were from lung cancer and 15% from 

asbestosis. The risk of death for asbestosis, at equal times from 

onset of exposure, was very similar in the miners and millers to 

that found in the factory workers and insulators. Lung cancer 

was similar among the miners and millers and in the factory 

workers but higher in the insulators. One death from mesothelioma was reported in this study. 

Selikoff (1977 b) surveyed 485 current employees of a 

chrysotile mine in Baire-Verte, Newfoundland, which had been 

in operation since 1963. Fifty employees (10%) had one or more 

radiographic abnormalities of the type commonly associated 

with asbestos exposure. Parenchymal abnormalities were most 

common, and pleural changes were detected in only 3% of the 

individuals surveyed. For those individuals employed less than 

5 years the prevalence of abnormalities was 5%, and this increased with duration of employment. Changes occurred most 

commonly in those with the most intense exposures. This study 

was designed only to assess asbestos-related disease under 

more modern conditions than have previous studies (Kogan et 

al., 1972; Rossiter et al., 1972); thus, assessments of the effects 

of short duration of exposure and long latency could not be 

made. The interpretation of these data is further complicated 

19 
by the lack of a control population and environmental measurements. The study does demonstrate the prevalence of chest 

X-ray changes in an appreciable proportion of employed workers, despite a short period since initial exposure. 

Rubino et al. (1979) reported nine asbestosis deaths among 

chrysotile asbestos miners in northern Italy. Excess lung cancer (7 vs. 3.4) was seen only during the last quinquennium of 

observation, 1971-1975, that period of time after greatest latency. Also, one mesothelioma was reported in this latest period. 

Studies examining lung tissue of mesothelioma cases and 

comparison groups have shown equivocal results as to the possible relationship of chrysotile in lung tissue and mesothelioma. Jones et al. (1979) found no evidence to indict chrysotile, 

while Acheson and Gardner (1979) estimated a 6-fold relative 

risk of mesothelioma for persons with only chrysotile in lung 

tissue as compared with controls with no asbestos fiber in 

their lungs. 

Boutin et al. (1979) reported on a study of chest film abnormalities among chrysotile miners and millers in Corsica. They 

studied 166 ex-workers of the mines and mill closed in 1965, and 

compared them with 156 controls without asbestos exposure 

and with similar demographic variables. Chest films were read 

according to the ILO U/C Classification system. Compared with 

controls, chrysotile workers had a prevalence of all parenchymal abnormalities 2.4 times that of controls. For those with a 

profusion of 1/2 or more, the prevalence ratio was approximately twice the controls. Pleural changes were twice as prevalent 

in chrysotile workers as in controls. Exposures among this cohort were reported to have been very high, with exposure levels 

ranging from 85 to 267 millian parts per cubic foot (mppcf). 

Crocidolite 

Jones et al. (1976) reported a high incidence of mesothelioma among women who worked predominantly with crocidolite 

in a factory producing gas mask canisters during World War II, 

and have recently extended observations on this population 

(Jones et al., 1979). Among this group of 1,088 workers exposed 

only between 1940 and 1945, 22 pleural and 7 peritoneal mesotheliomas were observed. This is likely an underestimate since 

373 women were lost to observation. A linear dose-response 

20 
relationship with length of employment was observed for mesothelioma, with three mesotheliomas observed among those exposed 5-10 months. 

McDonald and McDonald (1978) have also studied mortality 

of 199 workers exposed to crocidolite during gas mask manufacture in Canada during 1939 to 1942. This cohort was followed 

through 1975, and 56 deaths occurred. Out of these 56 deaths, 

4 (7%) were from mesothelioma and 8 from lung cancer. It 

should be pointed out that an additional five mesotheliomas not 

reported on death certificates were diagnosed on review of pathology or autopsy material. 

Mixed Fiber Types 

Weill et al. (1979) and Hughes and Weill (1979) reported on 

the mortality experience of a cohort of 5,645 men employed in 

production 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 persons were identified as deceased by the Social 

Security Administration. Those with unknown vital status 

(25%) by this source were assumed to be alive, thus likely 

resulting in underestimation of the true risk. Death certificates 

were obtained for 91 % of the known deaths. Dust exposures 

were estimated using each worker's employment history in conjunction with historical industrial hygiene data. 

Weill et al. (1979) observed increased respiratory cancer 

mortality only among those with exposure in excess of 100 

mppcf/year, where 23 cases were observed versus the 9.3 expected. The unusually low SMR for all causes in the low exposure groups suggests the possibility of a selection bias, and any 

interpretation of risks at low exposures should be done with 

caution. Two pleural mesotheliomas were reported. Separating 

the cohort by type of fiber exposure, the authors concluded that 

the addition of crocidolite to chrysotile enhanced the risk for 

respiratory malignancy; however, an excess risk (8 observed vs. 

4.4 expected) was observed among those not exposed to 

crocidolite, with cumulative exposures in excess of 200 mppcfmonths (16.6 mppcf-years). Both average concentration of 

exposure and durationlof exposure were found to be related to 

cancer risk. 

Jones et al. (1979) studied the progression of radiographic 

abnormalities and lung function among asbestos cement work21 
ers. Chest films taken in 1970 and 1976 on 204 workers were 

read independently by two readers according to the ILO U/C 

1971 Classification scheme. These films were read side-by-side 

in known order and ranked according to progression. Spirometric measurements were made in 1973 and 1976. The major 

findings of the Jones et al. study were: (1) the progression of 

small opacities was dependent upon both average and cumulative exposure; (2) significant declines in lung function were 

shown to result from both smoking and cumulative exposure; 

and (3) pleural abnormalities progressed as a function of time 

with little association to additional exposure. No estimates 

were made of the incidence of various respiratory abnormalities 

in relation to exposure. 

Peto (1979) reported on the mortality experience of a cohort 

of asbestos textile workers previously studied by Do'll (1955), 

Knox et al. (1968), and Peto et al. (1977). Data from this factory 

had previously been used by the British Occupational Hygiene 

Society (BOHS, 1968) in establishing occupational exposure 

standards and was subsequently studied by Lewinsohn (1972). 

Routine dust measurements in this factory were first made in 

1951. Among the 255 males first employed after 1951, 12 lung 

cancers were observed, whereas only 4.65 were expected, based 

on national death rates. Among those with 20 or more years 

since initial employment, 8 lung cancers were observed versus 

1.62 expected. Fiber exposures were estimated to be 32.4 

fibers/cc in 1951, decreasing to 1.1 fibers/cc in 1974. These estimates are 2.4 times previously estimated values for this plant 

(Peto et al., 1977). Peto estimated the relative risk for cumulative exposures of 200-300 fibers/cc-year to be between 2 and 3. 

The cohort is too small and followup too short to estimate cancer 

risks at lower exposures. No mesotheliomas were observed in 

the cohort first employed after 1951; however, the followup 

period is insufficient to address this question. 

Berry et al. (1979) extended their 1968 observations concerning asbestosis by including persons completing 10 or more 

years employment by 1972. Persons who left after June 30, 

1966, were also contacted and encouraged to participate, with 

68 of 113 persons eventually participating. Outcome measures 

studied included chest radiographs, medical examination including assessment of basal crepitations, and pulmonary function (FEV, FVC, FRC, TLC, RF, TL, PaC02). Chest films were 

read by four readers by the ILO/UC 1971 Classification system 

22 
with readings being averaged. Dust exposures were estimated 

for each person using available hygiene data and estimates of 

control effectiveness. 

In this study, "possible asbestosis" was diagnosed based on 

one or more combinations of basal rales or crepitations, radiological changes, a falling transfer factor, and restrictive lung 

function changes. Among these 379 men, 60 cases of possible 

asbestosis were diagnosed by the factory medical officer, whereas 85 cases were diagnosed by an independent clinician. Collaboration by these investigators subsequently resulted in 82 men 

with crepitations, 58 with "possible asbestosis," and 34 with 

certified asbestosis. Using the exposure data, these authors 

estimated the cumulative dose necessary for a 1 % incidence for 

crepitations, possible asbestosis, and certified asbestosis to be 

43, 55, and 72 fibers/cc-year, respectively. These authors pointed out limitations of the cumulative dose concept and acknowledged the imprecision of their exposure estimates. Two cases of 

certified asbestosis were observed among non-smokers and nine 

among ex-smokers. There were, in general, fewer respiratory 

symptoms and signs in non-smokers and light smokers than in 

heavy and ex-smokers. 

Elmes and Simpson (1977) have extended their earlier 

(1971) report to include deaths occurring since 1965 through 

1975. The mortality trend has shifted from a preponderance of 

asbestosis and gastrointestinal cancer deaths to malignancies 

of the lung and mesothelioma, diseases associated with longer 

latent periods. These authors stated that their findings would 

suggest any standard based "on the prevention of asbestosis 

may not provide adequate protection against neoplasia." 

Morbidity and mortality analysis by Lacquet et al. (1979) 

of workers in a Belgian asbestos cement factory revealed a 

strong dose-response relationship for asbestosis, and pleural 

and parenchymal lung changes. Pleural thickening and adhesions began occurring in the lowest dose category (0-49 

fibers/cc-year). Parenchymal lung changes occurred less frequently. No cases of asbestosis were recognized in workers with 

less than 100 fiber-years of exposure. Asbestosis occurs more 

frequently and with shorter latency periods (as the exposure 

levels increase) and adverse mortality tends to occur at longer 

latency periods (as the dose decreases) (Seidman et al., 1979). 

Because the observation period of the Lacquet et al. study was 

only 15 years,· it cannot be assumed that the absence of asbestosis in the low dose categories currently observed will not occur 

23 
in these low dose categories after a longer latent period, or that 

pleural and parenchymal lung changes are not indicators of 

early lung change that can or will progress to asbestosis. The 

mortality portion of the study revealed asbestosis and an excess 

of digestive cancer, but not excesses for lung cancer or mesothelioma. This, again, is not surprising since lung· cancer and 

mesothelioma tend to develop after latent periods greater than 

15 years. · 

Baselga-Monte and Segarra's (1978) examination of 1,262 

workers employed in four factories in the Barcelona area demonstrated a dose-response relationship based upon radiologic 

images. The authors demonstrated a quick response for pleural 

radiological changes at individual cumulative doses as low as 5 

fibers/cc-years, while the pulmonary and pleuropulmonary responses tend to appear later, but not at statistically different 

doses. The authors were reluctant to draw conclusions because 

of the design of the epidemiologic evaluation, which considered 

only active employees. Other epidemiologic studies of worker 

populations would indicate that evaluation of only active employees tends to underestimate the health risk since diseased 

workers oftentimes tend to self-select out of the active workforce (Fox and Collier, 1976; Enterline et al., 1972; Borow et al., 

1973). Baselga-Monte and Segarra concluded that "the present 

worldwide trend to establish more exigent hygienic criteria for 

exposure to asbest(os) is confirmed." Based on their working 

model, this level for a 50-year working life should be 0.07-0.10 

fiber/cc, "(taking into account protection levels of 89 and 95%)." 

Malignant Neoplasms other than Mesothelioma and Cancer of the Lung. 

A number of epidemiological studies indicate less striking associations of excess risks of other types of cancers (in 

addition to bronchial and mesothelial) and occupational asbestos exposure. Selikoff (1977a) reported increased rates for cancer of the stomach and esophagus (20 observed vs. 6.46 expected) and cancer of colon (23 observed vs. 7 .64 expected) among 

632 asbestos insulation workers in the New York and New 

Jersey area. Selikoff et al. (1979) made similar observations 

among 17,800 asbestos insulation workers in the United States 

and Canada. They reported increased mortality from cancer of 

the esophagus (18 observed vs. 7.1 expected), stomach (18 observed vs. 14.2 expected), and colon and rectum (58 observed vs. 

38.1 expected) among this study cohort. Similar observations 

24 
have been reported by others (Elmes and Simpson, 1971; Kogan 

et al., 1972). 

Cook and Olson (1979) have recently shown that sediment 

in human urine contains amphibole fibers, thus providing the 

first evidence that mineral fibers pass through the human gastrointestinal mucosa under normal conditions of the alimentary canal. 

Stell and McGill (1973) found that of 100 men with 

squamous-cell carcinomas of the larynx, 31 had known exposure to asbestos, compared with only 3 in matched controls. 

Similar associations have been reported by Morgan and Shettigara (1976); Shettigara and Morgan (1975); Rubino et al. (1979); 

and Selikoff et al. (1979a). Newhouse et al. (1979), however, 

utilizing an interview of patients at the Royal National Throat, 

Nose, and Ear Hospital in London, found that asbestos exposure 

was not more common among cases as compared to controls. 

Significant increases in cancer of the buccal cavity and of 

the pharynx have been reported by Selikoff et al. (1979a). 

Among 17,800 asbestos insulation workers they observed 16 

deaths due to cancer of these sites whereas 10.1 deaths would 

have been expected based on U.S. white male rates. 

Robinson et al. (1979) 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 7 deaths due to cancer of 

these sites, while 3.28 cases were expected. 

V. SMOKING AND ASBESTOS 

Hammond et al. (1979) recently reported the results of 

their 10-year followup study (January 1, 1967-December 31, 

1976) of 12,051 asbestos insulation workers who had 20 or more 

years of work experience. They were able to obtain complete 

smoking histories of a large number of study subjects (8,220 

workers) and compare their lung cancer mortality with that of 

a control population with a known smoking history. As a control population, 73,763 men in the American Cancer Society's 

prospective cancer prevention study were selected. These men 

were similar to asbestos workers in many respects. They were 

white males; non-farmers; had no more than a high school 

education; had a history of occupational exposure to dust, 

fumes, vapors, gases, chemicals, or radiation; and were alive as 

of January 1, 1967. Most of all, their smoking habits were 

also known. 

25 
Age-standardized lung cancer mortality rates for control 

and asbestos workers were as follows: 

History of 

Exposure cigarette Death* 

Groups to asbestos smoking rate 

Control No No 11.3 

Asbestos Yes No 58.4 

workers 

Control No Yes 122.6 

Asbestos Yes Yes 601.6 

workers 

*Rates per 100,000 man-years standardized for 

age on the distribution of the man-years of all 

the asbestos workers. Number of lung cancer 

deaths based on death certificate information. 

Mortality 

ratio 

1.00 

5.17 

10.85 

53.24 

Asbestos workers who did not smoke showed about a 5 times 

greater risk of dying of lung cancer when compared to the 

non-smoking control population. Asbestos workers who did 

smoke also had a 5 times greater risk of dying oflung cancer as 

compared to the controls who smoked. This means the relative 

risk associated with asbestos is about 5-fold for smokers and 

non-smokers alike. Therefore, the probability that their lung 

cancer was due to asbestos exposure is about 80% in both smokers and non-smokers. 

The combined effect of smoking and asbestos exposure appears to be more than simple addition. If the combined effect 

y,rere additive, one would expect death rates of 169.7 per 100,000 

man-years among asbestos workers who smoked. This rate was 

derived from the sum of the baseline rate (11.3) plus the excess 

over that baseline due to asbestos (58.4-11.3=47.1) plus the 

excess due to smoking (122.6-11.3=111.3). The data seem rather 

to satisfy a multiplicative model. It was shown that smoking 

alone increased the death rate about 11 times, and asbestos 

alone increased it 5 times. Therefore, for a multiplicative model, the mortality ratio for those exposed to both asbestos and 

smoking would be 55 (5 times 11) times greater than those who 

26 
were exposed neither to asbestos nor to smoking. The mortality 

ratio for those exposed to asbestos and to cigarettes was actually 53.24. 

Liddell et al. (1977) further analyzed the mortality experience of a cohort of chrysotile asbestos miners and millers previously studied by McDonald et al. (1973, 1974) and McDonald 

and McDonald (1976). This cohort of 10,951 men born between 

1891 and 1920, and who had at least 1 month of employment, 

was followed through December 31, 1973. Cause of death was 

ascertained for 97% of the 4,037 known deaths, whereas 1,117 

(10%) were lost to followup. Smoking habits were ascertained 

through a questionnaire administered to those living or to relatives of deceased workers who died after 1951. Unlike previous 

reports on this cohort, person-years were accumulated by 

5-year age groups and 5-year periods of calendar time, with 

expected deaths by cause calculated using mortality rates for 

males in the Province of Quebec. 

For this cohort, the SMR for all causes was 107, and a SMR 

of 125 was observed for cancer of the lung and pleura. There 

also were 40 pneumonoconiosis deaths. Using the whole cohort 

as the referent population, an excess of respiratory cancer was 

observed only after cumulative exposures of 300 mppcf-years 

(relative risk= 1.39). However, only 15 of the 40 pneumonoconiosis deaths occurred with exposures greater than 300 

mppcf-years. When available smoking data were taken into 

account, lung cancer Sl\1Rs o~ 48 and 46 were calculated 

for non-smokers and ex-smokers, increasing to 206 for heavy 

smokers. There were seven mesothelioma deaths among 

the cohort. 

The Liddell et al. study suffers in that an "unexposed" 

group is not used for dose-response analyses of lung cancer; 

thus, risk at low doses could not be estimated. Secondly, 

smoking-specific death rates were not used for calculation of 

expected lung cancer deaths, thus underestimating risks 

among non-smokers. 

There is little or no evidence that cigarette smoking is 

related to increased risk of pleural or peritoneal mesothelioma 

(Hammond et al., 1972, 1979). 

Data from two studies suggest that cigarette smoking 

may contribute to the risk of asbestosis. Hammond et al. (1979) 

reported that the asbestosis death rate of asbestos workers 

who smoked was 2.8 times as high as that of non-smoking 

27 
asbestos workers. Weiss (1971) reported a prevalence of pulmonary fibrosis of 40% (30/75) among asbestos workers who 

smoked in contrast to a prevalence of 24% (6/25) among nonsmoking asbestos workers. 

A small experimental study indicated that the particle 

clearance in the smokers was considerably slower than in the 

non-smokers. Cohen et al. (1979) reported that after a year 50 

percent of magnetic dust (Fe30 4) originally deposited remained 

in the lungs of the smokers while only 10 percent rernained in 

the lungs of the non-smokers. The authors suggested that 

smoking may impair the clearance of other dusts, including 

those that are toxic. This may help to explain the higher incidence of lung disease in smokers. 

In summary, both asbestos and smoking are independently 

capable of increasing the risk of lung cancer mortality. When 

exposure to both occurs, the combined effect with respect to 

lung cancer appears to be multiplicative rather than additive. 

From the evidence presented, we may conclude that asbestos is 

a carcinogen capable of causing, independent of smoking, lung 

cancer and mesothelioma. 

VI. EXPOSURE TO ASBESTIFORM MINERALS 

OTHER THAN COMMERCIALLY MINED 

ASBESTOS 

Gillam et al. (1976) reported a threefold excess risk of 

mortality from respiratory cancer and a twofold excess of nonmalignant respiratory disease (excluding influenza and pneumonia) among miners exposed to amphibole fibers in the 

cummingtonite - grunerite ore series at concentrations less 

than 2:0 fibers/cm3

• A large majority of the airborne fibers was 

shorter than 5 μmin length. McDonald et al. (1978), in a subsequent study of the same mine, examined the mortality experience of persons with at least 21 years of employment at the 

mine and mill. This study showed significant excesses of pneumoconiosis (mainly . silicosis), tuberculosis, and heart disease. 

No overall excess of malignant diseases was found. However, 

when the population was broken down by estimated exposure, 

respiratory cancer was in excess in the highest exposure group. 

The findings of McDonald et al. do not negate those reported by 

Gillam et al., but, rather, tend to strengthen them in that 

McDonald et al. used a rigid survival criteria (inclusion only of 

28 
those employed 21 or more years), and further diluted the underground exposed effect by including persons never exposed 

underground. 

Commercial talc deposits are sometimes found to contain 

serpentines (chrysC'tile, antigorite, and lizardite) and fibrous 

and non-fibrous amphiboles. One important deposit studied has 

been mined in the Gouveneur Talc District of upper New York 

State. Talcs in this area contained less than 1-2% silica, but 

have been shown to contain tremolite and anthophyllite, 

resulting in elevated miner and miller exposures to these fibers 

(Dement and Zumwalde, 1979). 

Kleinfeld et al. (1967, 197 4) demonstrated elevated proportionate mortality due to lung cancer and respiratory disease 

among talc miners and millers in New York State. Brown et al. 

(1979) conducted a retrospective cohort mortality study among 

workers of one company in this area. The study cohort consisted of all white males initially employed sometime between 

January 1, 1947 and December 31, 1959, with followup through 

June 30, 1975. Expected cause-specific deaths were calculated 

using age, calendar time, and cause-specific mortality rates of 

the U.S. Among this cohort, 10 respiratory cancers were observed, whereas only 3.5 were expected. Excess mortality was 

also observed for non-malignant respiratory diseases. One case 

of mesothelioma was observed; however, this worker was 

known to have had prior employment with unknown exposures 

in the construction industry. 

Gamble et al. (1979) studied respiratory disease morbidity 

among a cohort employed at the same mine and mill studied by 

Brown et al. (1979). A total of 121 currently employed workers 

were given a respiratory questionnaire, PA and lateral chest 

films, and spirometry tests. Talc workers with greater than 15 

years employment were found to have an increased prevalence 

of pleural abnormalities compared to coal miners, potash miners, and chrysotile asbestos workers. FEV1 and FVC reductions 

demonstrated significant association with particulate and fiber 

exposure. 

Mesothelioma of the pleura and peritoneum have been detected in two villages in Turkey: Tuzkoy and Karain (Artvinli 

and Baris, 1979 and Baris et al., 1978). Mineralogical analysis 

of samples from ore and water has revealed the asbestiform 

mineral zeolite but no asbestos. These fibers were usually 

1-2 μmin diameter and 30-40 μmin length. Annual rates of 

29 
malignant pleural mesothelioma in Tuzkoy were found to be 22 

cases per 10,000 people, and 182 cases per 10,000 in Karain, 

while studies in Pennsylvania (Lieben and Pistawka, 1967), 

Finland (Nurminen, 1975), and England, Wales, and Scotland 

(Greenberg and Davies, 197 4) reported annual incidences of 1 to 

2.3 cases per 1,000,000 persons. 

VII. NON-OCCUPATIONAL EXPOSURE TO 

COMMERCIAL SOURCES OF ASBESTOS 

Anderson et al. (1979) reported on the occurrence of X-ray 

abnormalities among household contacts of workers in an amosite asbestos factory. The study cohort consisted of 679 household contacts who had lived in the household of an actively 

employed amosite asbestos factory worker and who themselves 

had not had occupational exposure to asbestos or other fibrogenic dust. These individuals were given a PA chest film which 

was read by five readers according to the 110/UC Classification 

of 1971. For comparison, 325 controls living in the same community as the study subjects, matched by age and sex, were 

examined. 

Among the study population, there was a 17% prevalence 

of small opacities, versus 3% for the controls. Pleural calcifications were present in 8% of the household contacts and were 

seen in none of the controls. There were 35% with one or more 

radiological abnormalities among household contacts in contrast to 5% among controls. An increasing prevalence of all 

abnormalities with duration of exposure was observed. 

Churg et al. (1978) reported a case of mesothelioma of the 

pericardium in a man treated 15 years earlier for angina pectoris by dusting of the pericardia! cavity with a mixture of fibrous 

dusts including anthophyllite asbestos, tremolite asbestos, and 

fibrous glass. 

VIII. DOSE-RESPONSE RELATIONSHIPS 

Evidence available to date indicates that a large dose of 

asbestos will produce a bigger health hazard than a small dose. 

Seidman et al. ,(1979), using the length of time worked in an 

amosite asbestos factory as a measure of the dosage of asbestos, 

reported an increased risk of dying from lung cancer with increasing duration of employment. Henderson and Enterline 

(1979), using cumulative dust exposure as an estimate of dose, 

30 
reported that the dose-response relationship for lung cancer is 

more likely linear. They predicted the relationship to be 

SMR=l00+0.658 times cumulative dust exposure (mppcfyears). Liddell et al. (1977) also reported a similar relationship, 

i.e., a tendency for the mortality for lung cancer to increase 

with the dose. 

Berry et al. (1979) reported that the occurrence of crepitations, possible asbestosis, and certified asbestosis was related to 

the cumulative dose. 

Newhouse and Berry (1973) suggested that the risk of 

dying from mesothelioma increases with increasing dose. Jones 

et al. (1979) reported a linear relationship between the mesothelioma rate and length of exposure. In a study of the women 

workers in a wartime gas mask factory, they found that women 

having a long employment period had a higher proportion of 

death due to mesothelioma than those who had a short period 

of employment. 

Although there appears to be little dispute that a larger 

dose of asbestos will pose a greater health risk, the exact nature 

of the dose-response relationships may be subject to considerable debate. This is so primarily because of problems of exposure 

estimation. Methods of measuring dust levels have changed 

over time with respect to sampling instrument (thermal precipitation vs. midget impinger vs. membrane filter), location of 

sampling (personal vs. area), and dust counting (particles vs. actual fibers) and/or evaluation techniques (whole fields vs. eyepiece 

graticule). As a result, conversion of dust levels obtained by one 

method to levels comparable to another method is far from 

simple, and is subject to considerable error. Another factor 

which may lead to differences of opinion on the exact shape of 

the dose-response curve is the measure of the dose. The commonly used measures of exposure are the cumulative dose and 

the duration of employment. Since using cumulative dose as a 

measure of exposure gives equal weight to the concentrations of 

dust experienced in each year of exposure, exposure of many 

years ago is considered as important as recent exposure. This 

practice is unrealistic for the chronic diseases having a long 

la.tency period. Duration of employment has also been used as 

a measure of exposure under the assumption that increasing 

the work time approximates increasing the dose. This procedure has the same problem as using the cumulative dose. Fur31 
thermore, in the absence of reliable past exposure data, 

the duration of employment may not equal the total dose of 

asbestos. 

With regard to the linear hypothesis, the British Advisory 

Committee on Asbestos stated the following in 1979: 

Our reasons for preferring a linear hypothesis are: 

(1) It fits the data for occupational exposures; 

(2) it is the simplest hypothesis and the one most readily used for extrapolation to the 

probable effects of low doses; (3) it is likely to 

lead to an overestimate rather than underestimate of risks at very low doses. (Final Report, 

Vol. 2, p. 14). 

Data available to date provide no evidence for the existence 

of a threshold level. Virtually all levels of asbestos exposure 

studied to date demonstrated an excess of asbestos-related 

disease. 

32 
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