Workplace Exposure to Asbestos:
Review and Recommendations
BIOLOGIC EFFECTS OF
EXPOSURE TO ASBESTOS
IN ANIMALS
Memorandum on Asbestos Update and Recommended
Occupational Standard
I. Asbestos Nomenclature/Definitions
II. Asbestos Sampling and Analysis
III. Biologic Effects of Exposure to
Asbestos in Animals
IV. Biologic Effects of Exposure to
Asbestos in Humans
V. Smoking and Asbestos
VI. Exposure to Asbestiform Minerals
other than Commerically Mined Asbestos
VII. Non-Occupational Exposure to Commerical
Sources of Asbestos
VIII. Dose-Response Relationships
References
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.
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 inhalation
exposures (Wagner et al., 1974). In terms of degree of response 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 mcm in 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 and diameters, Stanton et al. (1977)
were able to show that glass fibers with diameters less than 1.5 mcm and
lengths greater than 8 mcm 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
mcm in diameter induced pleural sarcomas in 64% of rats, whereas another
preparation in which only 16% of the fibers were less than 1.5 mcm in
diameter induced pleural sarcomas in only 14% of rats. Ninety-five percent
of the fibers in both preparations were greater than 8 mcm in length.
Besides the corroborating evidence for the carcinogenic potential of
asbestos, recent results indicate a strong co-carcinogenic 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 neoplasms 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.
Memorandum on Asbestos Update and Recommended
Occupational Standard
I. Asbestos Nomenclature/Definitions
II. Asbestos Sampling and Analysis
III. Biologic Effects of Exposure to
Asbestos in Animals
IV. Biologic Effects of Exposure to
Asbestos in Humans
V. Smoking and Asbestos
VI. Exposure to Asbestiform Minerals
other than Commerically Mined Asbestos
VII. Non-Occupational Exposure to Commerical
Sources of Asbestos
VIII. Dose-Response Relationships
References
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