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G. Berry, J. C. Gilson, S. Holmes, H. C. Lewinsohn, and S. A. Roach
Asbesto
Most of the men in the study had been employed elsewhere before starting work at the factory; only 40% started before age 30. Of the 13 men in the post-1950 group who had possible asbestosis, five had worked in the cotton industry. One of these had been a stripper and grinder for 20 years and was considered to have reached the possible asbestosis category within eight years of first employment at the factory studied, the only sign within 10 years (Table 2). Another man who was certified as suffer ing from asbestosis after 12 years in the factory had previously been a chemical worker for 20 years; asbestosis was not confirmed at death. It seems likely,
clues to the most appropriate value of the half-ljfe time of dust elimination. If elimination were slow then cases of asbestosis would be first diagnosed and certified in men who left the industry many years earlier; if this were not the case, then the use of cumulative dose would be reasonably valid. It is known that an excess incidence of lung cancer and mesothelioma occurs in men many years after the end of exposure (Newhouse, 1973) but infoimation is lacking on the diagnosis of asbestosis in former asbestos workers.
There are several reasons why the models might be inappropriate. First, if the diagnostic procedures
'
cumula the pre in thosi standar Crepita
nor woi disease, Possibh be eitht correlat group fi ive expi since fit
therefore, that some of the signs observed in this were not uniform over the period 1961-73, then study were at least partly attributable to previous some of the recorded new cases could be attributable
of poss findings
employment in other dusty occupations.
to a change in diagnostic criteria rather than to true
2f/cm3
The association between smoking and signs of clinical changes. The factory medical officer was
to redui
asbestosis (Table 6) is in agreement with Weiss (1971) replaced during this period and, in addition, lung
At this
who found pulmonary fibrosis in the chest radio function testing was introduced at about the same . the star
graph in 40% of smokers and 24% of non-smokers time. Second, the assumption that the amount of
is so re
among workers exposed to chrysotile asbestos.
dust deposited in the lungs is a fixed proportion of the
exposed
The data have been analysed in terms of a family airborne concentration would not be valid if there
necessai
of exposure measures, an inherent feature of which had been changes in the particle size in the airborne
1 is that there is the equivalent of an exponential dust cloud during the period 1951-72. In view of the decline in the amount of active material. This could changes in dust levels over this period, a change in
We are Springe
arise as a result of both elimination of dust and a the size distribution would not be surprising; how
two ret
reduction in activity of the dust remaining. Beattie ever we have no relevant data.
Dempst
and Knox (1961) determined the mineral content
A dose-response relationship between morbidity
Mcdica
after death in lungs of workers from the factory, and asbestos exposure has been considered in two
Dr P. C
and found no evidence of a decline in the first eight other studies. McDonald et al. (1974) studied
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years after exposure had stopped. However, they several facets of disease, death, radiological changes,
to Dr J.
I.
took no account of changes in dust level; those who pulmonary function changes and respiratory symp had survived for a period after leaving the factory toms and related these to the cumulative exposure
to Mr i respons
were, on average, probably first exposed about measured as millions of particles per cubic foot : post-mc
15 years earlier than those who died while still times years (mpcf-yr). They concluded that there , and enc
employed, and 70% of the men in the study had was a 1% risk of acquiring clinically significant been employed before 1932. There is evidence that disease for an exposure between 100 and 200 mpcf-yr.
Rcfcrenci
trace metals are leached from chrysotile asbestos Some of their observations were based on a complete
Beattie, J
in vivo (Morgan et al., 1971; Morgan et al., 1973). This leaching, and other changes within the lungs, may reduce the hazard of the remaining material. The range of measures was introduced because it
cohort but others only on current employees. Weill et al. (1975) considered lung function measurements and irregular small opacities on the chest radiographs and found little evidence of a dose-response relation
and pi textile pp. 41i Oxforc Berry, G.
was felt that the simplest measure, that of cumulative exposure, might not be completely satisfactory because of its inability to allow for the possibility of development of disease after exposure has ended. Crepitations appeared to develop in five men while they were not exposed, but in two of these the change could have been caused by observer differences. The changes in the other three men could have been attributable to the transient nature of the sign or to reasons other than asbestos exposure.
Because so few of the men have been retired for even five years, we are unable to discriminate between the different dose-response relationships. Data of this type from other sources would provide
ship below 100 mpcf-yr. Using the results of simul taneous sampling with the impinger and fibre counting method they equated this dose with 200 f-yr/cms. Their observations were based on current employees only, and for some, exposure
had started only shortly before the study. The results of the present study are disappointing
in that it is not possible to draw any definite con clusions on the effects of the present 2f/cms standard. Comparison of the present results with those given earlier (British Occupational Hygiene Society, 1968; Berry, 1973) shows that there is a higher prevalence of crepitations at any dose than was observed previously. However, in view of the doubt that
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Dreessen J. W,, (1938).