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1/8/2009
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| Our 1990 article reported on recent papers in the peer-reviewed literature and
two international symposia, one at the International Agency for Research on
Cancer (2) and the other at Harvard University (3), all concluding that
chrysotile fibers are less active than amphibole types (crocidolite, amosite,
tremolite) of asbestos in the causation of mesothelioma in man. In his summary
of the IARC meeting, Sir Richard Doll, an eminent epidemiologist, concluded
there is the difference between the effects of chrysotile and amphiboles, which
is so great in relation to mesothelioma that it is possible to argue that
chrysotile does not cause mesothelioma at all (2). This observation has been
supported by numerous peer-reviewed papers and working groups subsequently
(4-6). |
| Mesothelioma, a fatal cancer usually found on the lining of the lung, is
specifically recognized in Ontario—as is asbestosis—as arising from
exposure to asbestos. Mesothelioma is written into the Compensation Act
as a Schedule 4 Disease. |
| In stating that a threshold of effect has never been found for asbestos, Rall
stands behind the outdated one fiber can kill theory of carcinogenesis.
However, Rall fails to mention data supporting a threshold for chrysotile in
lung cancer (11, asbestosis (12), and mesothelioma (13) as well as a panel
report from the Health Effects Institute-Asbestos Research (HEI-AR) detailing
animal and in vitro dose-response studies exhibiting no-observed adverse effect
levels (NOAELs) for asbestos (14). Our recent work documents a dose-dependent
increase in asbestos-induced proto-oncogene activation in mesothelial cells with
no induction at lowest concentrations of fibers tested and an enhanced potency
of crocidolite asbestos in comparison to chrysotile (15). |
| Latency periods (time intervals elapsing between first exposure to
asbestos and death) were examined in 421 cases of
malignant pleural mesothelioma, diagnosed in the Trieste-Monfalcone
area, Italy. Occupational data were collected from the
patients or from their relatives by personal or telephone interviews.
Routine lung sections were examined for asbestos bodies in
370 cases. Latency periods, calculated in 312 cases, ranged from 14
to 72 years (mean 48.7, median 51). Latency periods
differed significantly from one occupational group to another. Mean
latency periods were 29.6 among insulators, 35.4 among
dock workers, 43.7 in a heterogeneous group defined as various, 46.4
in non-shipbuilding industry workers, 49.4 in shipyard
workers, 51.7 among women with a history of domestic exposure to
asbestos, and 56.2 in people employed in maritime
trades. The ANOVA test indicated a correlation between latency
periods an. |
| A series of 421 malignant pleural mesotheliomas, diagnosed in the
Trieste-Monfalcone area, northeastern Italy, were reviewed.
A large majority of the patients had been employed in naval work
(shipbuilding, maritime trades, and dock work). Latency
periods (time intervals between first exposure to asbestos and
death), showed wide variations from one occupational category
to another. Such variations were attributable, but only partly, to
differences in the intensity of the exposure to asbestos. Various
family cases were identified, including people with and without blood
relationships. The data, obtained in the studies on
Trieste-Monfalcone mesothelioma, suggest that interactions between
asbestos and other factors play a considerable role in the
pathogenesis of asbestos-related mesothelioma.
___________________________________________________________
Med Lav 1997 Jul-Aug;88(4):310-5 |
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