One interesting study
is called, “Insulation workers in Belfast. A further study of mortality due to
asbestos exposure (1940-75).” - Br J Ind Med 1977;34:174-180 – by P C Elmes, M
J Simpson. Here is an excerpt: “Abstract - A follow-up study of 162 men already
working as insulators (laggers) in 1940 has been extended from 1965 to 1975. By
the end of 1975 there were 40 survivors when 108 had been expected. Until 1965
there had been an overall excess of deaths; these were due to asbestosis with
or without tuberculosis and to alimentary cancer, as well as to bronchial
carcinoma and mesothelioma. From 1965 onwards the overall death rate among
survivors is not so excessive but there is still a marked excess of deaths from
bronchial cancer and mesothelioma. The continued risk of death attributable to
malignancy after asbestosis had ceased to contribute directly, does not appear
to be caused by any changes which occurred before 1940 in the conditions at
work.”
Another interesting
study is called, “Frequency of sister chromatid exchange and chromosomal
aberrations in asbestos cement workers.” - Br J Ind Med 1991;48:103-105 by N
Fatma, A K Jain, Q Rahman – Abstract “Exposure to asbestos minerals has been
associated with a wide variety of adverse health effects including lung cancer,
pleural mesothelioma, and cancer of other organs. It was shown previously that
asbestos samples collected from a local asbestos factory enhanced sister
chromatid exchanges (SCEs) and chromosomal aberrations in vitro using human
lymphocytes. In the present study, 22 workers from the same factory and 12
controls were further investigated. Controls were matched for age, sex, and
socioeconomic state. The peripheral blood lymphocytes were cultured and
harvested at 48 hours for studies of chromosomal aberrations and at 72 hours
for SCE frequency determinations. Asbestos workers had a raised mean SCE rate
and increased numbers of chromosomal aberrations compared with a control
population. Most of the chromosomal aberrations were chromatid gap and break
types.”
Another interesting
study is called, “Asbestos-Induced Pleural Disease” - Clinics in Chest
Medicine, Volume 19, Issue 2, Pages 311-329 by S.Nishimura, V.Broaddus. Here is
an excerpt: “Abstract - Asbestos, for unknown reasons, has an unusual affinity
for the pleura. The manifestations of asbestos-induced pleural disease are
multiple and varied, from effusion to fibrosis to malignancy. Certain types of
pleural disease, such as pleural plaques, are nearly specific for asbestos
exposure, whereas others, such as asbestos-induced pleural effusion, are
difficult to identify unequivocally as asbestos-related. Although much progress
on the basic mechanisms of asbestos-cellular interactions has been achieved,
the origin of pleural disorders remains unknown. Furthermore, the relationship
of the different pleural conditions with each other and with the pulmonary
manifestations of asbestosis and lung cancer are not understood. In this
article, we attempt to concentrate on the newer studies that offer answers to
some of the questions above. We refer readers to recent reviews on
asbestos-related pleural disease.26, 32, 43 and 52”
Another study is
called, “Pulmonary fibrogenesis after three consecutive inhalation exposures to
chrysotile asbestos” by PG Coin, AR Osornio-Vargas, VL Roggli and AR Brody -
Am. J. Respir. Crit. Care Med., Vol 154, No. 5, 11 1996, 1511-1519. Here is an
excerpt: “Previously, this laboratory developed a model of asbestos-induced
pulmonary fibrogenesis in rats and mice after a brief (1 to 3-h) inhalation
exposure. However, typical human environmental exposures would be repeated,
although at lower concentrations than those used in our animal model. Here we
have extended this model to encompass repeated exposures and consequent
long-term effects. Groups of rats were exposed to chrysotile aerosol (10 mg/m3)
for 3- to 5-h periods over 3 consecutive days. Lung fiber burden and pathologic
features were studied for as long as 6 mo after exposure. We found that many of
the longest (> or = 8 microm) fibers were retained in the lung for at least
6 mo, whereas shorter fibers were cleared more rapidly. The three exposures to
chrysotile caused a large increase in DNA synthesis in the epithelium of
terminal bronchioles and more proximal airways. When compared with a single
exposure, the triple exposure caused an enhanced inflammatory response as well
as a prolonged period of increased DNA synthesis in the proximal alveolar
region. Hyperplastic, fibrotic lesions subsequently developed in the same
region and persisted for at least 6 mo after exposure. These findings will be
valuable in directing future studies of the mechanisms of pulmonary fibrosis in
this model.”
If you found any of
these excerpts interesting, please read the studies in their entirety. We all
owe a debt of gratitude to these fine researchers.
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