Asbestos was mined in Australia for over one hundred years and Australia was the world’s
highest user per capita of asbestos in the 1950s. It is thus no surprise that in the 1980s and
1990s Australia has had the world’s highest incidence of malignant mesothelioma. While
this is not something to be proud of, it has probably led to one of the most complete studies
of the disease in the world. It is the purpose of this chapter to describe the history of mesothelioma
in Australia as a whole, with special reference to the Wittenoom crocidolite mining
operation in Western Australia. Material will be drawn from research studies conducted
over the last 20 years by the Australian Mesothelioma Program and Register (National Occupational
Health and Safety Commission and University of Sydney) and the University of
Western Australia. The chapter updates and enhances previous reviews
History of asbestos production and use in Australia
Between 1880 and 1889 approximately 47 tonnes of amphiboles were mined at Jones’
Creek, near Gundagai, New South Wales, and between 1890 and 1899 about 35 tonnes
of chrysotile was mined at Anderson’s Creek, Tasmania. South Australia was the first
State to mine crocidolite, at Robertstown in 1916.
Over the present century there was a gradual increase in asbestos production,
with more chrysotile than amphiboles mined until 1939. With the commencement of
mining at Wittenoom, Western Australia, in 1937, crocidolite dominated production,
until final closure in 1966. New South Wales, the first State to mine asbestos, also
produced the largest tonnages of chrysotile (until 1983) as well as smaller quantities
of amphiboles (until 1949).
With the closing of the crocidolite mine at Wittenoom in 1966, Australian asbestos
production declined to a pre-1952 level. Exports declined from 1967. Imports of
chrysotile also started to decline. The earliest records of asbestos imports date from
1929. The main sources of raw asbestos imports were Canada (chrysotile) and South Africa (crocidolite and amosite). About twice as much chrysotile was imported as was
mined and half as much crocidolite was imported as was mined. After Wittenoom was
closed, a small amount (122 tonnes) of crocidolite was mined in South Australia.
Australian production of asbestos fibre decreased in 1981 because of the drop in
world demand for asbestos and the increased operating costs at the Woodsreef mine.
This mine ceased production in 1983 when the dry milling plant could not meet dust
control regulations.
Details of Australian asbestos production and imports are shown in Tables 3.1 and
3.2. Australian asbestos (crocidolite and chrysotile) was exported to the USA, Japan, UK
and Europe. In particular, Wittenoom crocidolite was exported to the USA and Europe.
Longer chrysotile fibres were used in fireproof textiles, insulation materials, packing
and woven brake linings, among other products. Medium length fibres were used mainly
as fillers in various linings, facing, floor tiles and asphalts. Crocidolite, because of its high
tensile strength, was used in conjunction with chrysotile in the manufacture of asbestos
cement pressure pipes. The long fibres were also used for weaving into fabrics for use in
boiler laggings and acid-resistant gaskets. It was also used in lining pipes, tanks and other
vessels in the chemical industry and as a strengthening agent in epoxy and phenolic resins.
Exposures in the past were very high in some industries and jobs – up to 150
fibre/mL (e.g., 25 million particles per cubic foot in asbestos pulverisers and disintegrators
in the asbestos cement industry.7 High concentrations of fibres in mining occupations
were also recorded (up to 600 fibre/mL in baggers at Wittenoom).8
With this background, it was almost certain that Australia would suffer a mesothelioma
epidemic of a severe nature.
The first reported case, from Wittenoom, was in 1962.9 Three more cases were
reported from Victoria in 1966,10 two from Queensland in 196811 and a further nine
from Victoria in 1969.
Australian Mesothelioma Surveillance Program
The Australian Mesothelioma Surveillance Program (the program), as it finally became
known, endeavoured to correct most of the weaknesses identified in the 1960s
and 1970s in other such schemes throughout the world, viz, under-reporting of cases,
uncertain diagnosis, poor elucidation of the role of occupational and environmental
asbestos exposure and less than comprehensive coverage.13
The program began on 1 January 1980 after preliminary work from 1977. Formal
voluntary notification of cases was actively sought from a network of respiratory
physicians, pathologists, general and thoracic surgeons, medical superintendents,
medical records administrators, State and Territory departments of occupational health,
cancer registries, compensation authorities or any other source. Notifications from
other than the diagnosing physician were confirmed with him or her. After gaining the
appropriate consents a full occupational and environmental history was obtained for
each case, from either the patient or next-of-kin. The history taking was non-directive
but included specific questions on asbestos exposure at the end. These histories were
coded by two occupational hygienists, who naturally could not be blinded to case status.
They also discussed cases together and were thus not independent. The diagnosing
pathologist was requested to provide slides and/or tissue specimens. These were
circulated among a pathology panel for confirmation of diagnosis. Post-mortem examination
was actively sought for in every case in order to confirm diagnosis and to
obtain lung tissue free of tumour for lung fibre content analysis.
Occupational and environmental exposure was classified as definite, probable
and possible, based on the subjective opinions of the two hygienists. Occupation and
industry classifications were based on the Australian Bureau of Statistics Industry and
Occupation Codes. Further grading of intensity of exposure was also very subjective in
many cases and duration depended on recollection.
Year of presumptive diagnosis was the year in which mesothelioma was first suspected
clinically. Year of definitive diagnosis was the year when pathology panel diagnosis
was finalised. The panel of five members of the Royal College of Pathologists of
Australasia reported individually on the diagnosis as definite, probable, possible and
not mesothelioma. The level of consensus was good, with exact agreement or disagreement
of only one category in 94% of cases. A scoring system of 1 (definite), 0.75
(probable), 0.5 (possible) and 0 (not mesothelioma) was used and the definitive score
taken as the score nearest the mean of five. Panel members also classified mesothelioma
cell type as epithelial, sarcomatous, mixed or not agreed.
Lung fibre content was assessed by a local modification of a sodium hypochlorite
digestion and filter method. Both light and electron microscopy (with energy dispersive xray
analysis) were used. Fibres were counted by asbestos type and length but not diameter.
All fibre lengths were recorded but because of uncertainties about filter contaminants by
<2 micron fibres, only fibres >2 micron (EM) or >5 micron (LM) were considered in
analyses. These methods gave a sensitivity, corresponding to one fibre counted, of 15 000
fibre/g dry lung (LM) and 200 000 fibre/g dry lung (EM). Assuming a Poisson distribution
of fibres in the counting units, the upper limit of the 95% confidence interval for the population mean, given a zero count obtained, is 3.69. Thus the EM ‘detection limit’ is
about 740 000 fibre/g.14 Reports on lung fibre content levels were sometimes used for
medico-legal purposes in a fallacious way in that counts were reported as being ‘within the
normal range’ as if this excluded an occupational asbestos exposure and liability. The
‘normal’ range was in fact taken from urban hospital patients without mesothelioma and,
where fibres were counted, exposure obviously had been received (and not always environmental
only as judged by fibre length distribution, i.e., it must have sometimes been occupational
– no work histories were available). It was not realised until later that these patients
should rather be treated as non-cases (referents) in a case-referent study.
The incidence of mesothelioma in Australia
Incidence rates are periodically calculated on cases notified to the program. An annual
report series is produced (NOHSC, 1989–20006). Cases accepted by the pathology panel in
the program as definite, probable or possible are included. Because of delays in definitive
diagnosis being received, incidence rates have been calculated up to end 1996 only, because
of the up to two year delay in notification experienced while awaiting confirmed
diagnosis and reconciliation with the state cancer registries. Figure 3.3 shows age-specific
incidence for males and females >20 years of age for the year 1996. Figures 3.4 and 3.5
show age-specific incidence trends over time for males and females. Figures 3.6–3.8 show
trends in world population >20 years of age standardised mesothelioma incidence by State,
sex and site for recent years
History of asbestos production and use in Australia
Between 1880 and 1889 approximately 47 tonnes of amphiboles were mined at Jones’
Creek, near Gundagai, New South Wales, and between 1890 and 1899 about 35 tonnes
of chrysotile was mined at Anderson’s Creek, Tasmania. South Australia was the first
State to mine crocidolite, at Robertstown in 1916.
Over the present century there was a gradual increase in asbestos production,
with more chrysotile than amphiboles mined until 1939. With the commencement of
mining at Wittenoom, Western Australia, in 1937, crocidolite dominated production,
until final closure in 1966. New South Wales, the first State to mine asbestos, also
produced the largest tonnages of chrysotile (until 1983) as well as smaller quantities
of amphiboles (until 1949).
With the closing of the crocidolite mine at Wittenoom in 1966, Australian asbestos
production declined to a pre-1952 level. Exports declined from 1967. Imports of
chrysotile also started to decline. The earliest records of asbestos imports date from
1929. The main sources of raw asbestos imports were Canada (chrysotile) and South Africa (crocidolite and amosite). About twice as much chrysotile was imported as was
mined and half as much crocidolite was imported as was mined. After Wittenoom was
closed, a small amount (122 tonnes) of crocidolite was mined in South Australia.
Australian production of asbestos fibre decreased in 1981 because of the drop in
world demand for asbestos and the increased operating costs at the Woodsreef mine.
This mine ceased production in 1983 when the dry milling plant could not meet dust
control regulations.
Details of Australian asbestos production and imports are shown in Tables 3.1 and
3.2. Australian asbestos (crocidolite and chrysotile) was exported to the USA, Japan, UK
and Europe. In particular, Wittenoom crocidolite was exported to the USA and Europe.
Longer chrysotile fibres were used in fireproof textiles, insulation materials, packing
and woven brake linings, among other products. Medium length fibres were used mainly
as fillers in various linings, facing, floor tiles and asphalts. Crocidolite, because of its high
tensile strength, was used in conjunction with chrysotile in the manufacture of asbestos
cement pressure pipes. The long fibres were also used for weaving into fabrics for use in
boiler laggings and acid-resistant gaskets. It was also used in lining pipes, tanks and other
vessels in the chemical industry and as a strengthening agent in epoxy and phenolic resins.
Exposures in the past were very high in some industries and jobs – up to 150
fibre/mL (e.g., 25 million particles per cubic foot in asbestos pulverisers and disintegrators
in the asbestos cement industry.7 High concentrations of fibres in mining occupations
were also recorded (up to 600 fibre/mL in baggers at Wittenoom).8
With this background, it was almost certain that Australia would suffer a mesothelioma
epidemic of a severe nature.
The first reported case, from Wittenoom, was in 1962.9 Three more cases were
reported from Victoria in 1966,10 two from Queensland in 196811 and a further nine
from Victoria in 1969.
Australian Mesothelioma Surveillance Program
The Australian Mesothelioma Surveillance Program (the program), as it finally became
known, endeavoured to correct most of the weaknesses identified in the 1960s
and 1970s in other such schemes throughout the world, viz, under-reporting of cases,
uncertain diagnosis, poor elucidation of the role of occupational and environmental
asbestos exposure and less than comprehensive coverage.13
The program began on 1 January 1980 after preliminary work from 1977. Formal
voluntary notification of cases was actively sought from a network of respiratory
physicians, pathologists, general and thoracic surgeons, medical superintendents,
medical records administrators, State and Territory departments of occupational health,
cancer registries, compensation authorities or any other source. Notifications from
other than the diagnosing physician were confirmed with him or her. After gaining the
appropriate consents a full occupational and environmental history was obtained for
each case, from either the patient or next-of-kin. The history taking was non-directive
but included specific questions on asbestos exposure at the end. These histories were
coded by two occupational hygienists, who naturally could not be blinded to case status.
They also discussed cases together and were thus not independent. The diagnosing
pathologist was requested to provide slides and/or tissue specimens. These were
circulated among a pathology panel for confirmation of diagnosis. Post-mortem examination
was actively sought for in every case in order to confirm diagnosis and to
obtain lung tissue free of tumour for lung fibre content analysis.
Occupational and environmental exposure was classified as definite, probable
and possible, based on the subjective opinions of the two hygienists. Occupation and
industry classifications were based on the Australian Bureau of Statistics Industry and
Occupation Codes. Further grading of intensity of exposure was also very subjective in
many cases and duration depended on recollection.
Year of presumptive diagnosis was the year in which mesothelioma was first suspected
clinically. Year of definitive diagnosis was the year when pathology panel diagnosis
was finalised. The panel of five members of the Royal College of Pathologists of
Australasia reported individually on the diagnosis as definite, probable, possible and
not mesothelioma. The level of consensus was good, with exact agreement or disagreement
of only one category in 94% of cases. A scoring system of 1 (definite), 0.75
(probable), 0.5 (possible) and 0 (not mesothelioma) was used and the definitive score
taken as the score nearest the mean of five. Panel members also classified mesothelioma
cell type as epithelial, sarcomatous, mixed or not agreed.
Lung fibre content was assessed by a local modification of a sodium hypochlorite
digestion and filter method. Both light and electron microscopy (with energy dispersive xray
analysis) were used. Fibres were counted by asbestos type and length but not diameter.
All fibre lengths were recorded but because of uncertainties about filter contaminants by
<2 micron fibres, only fibres >2 micron (EM) or >5 micron (LM) were considered in
analyses. These methods gave a sensitivity, corresponding to one fibre counted, of 15 000
fibre/g dry lung (LM) and 200 000 fibre/g dry lung (EM). Assuming a Poisson distribution
of fibres in the counting units, the upper limit of the 95% confidence interval for the population mean, given a zero count obtained, is 3.69. Thus the EM ‘detection limit’ is
about 740 000 fibre/g.14 Reports on lung fibre content levels were sometimes used for
medico-legal purposes in a fallacious way in that counts were reported as being ‘within the
normal range’ as if this excluded an occupational asbestos exposure and liability. The
‘normal’ range was in fact taken from urban hospital patients without mesothelioma and,
where fibres were counted, exposure obviously had been received (and not always environmental
only as judged by fibre length distribution, i.e., it must have sometimes been occupational
– no work histories were available). It was not realised until later that these patients
should rather be treated as non-cases (referents) in a case-referent study.
The incidence of mesothelioma in Australia
Incidence rates are periodically calculated on cases notified to the program. An annual
report series is produced (NOHSC, 1989–20006). Cases accepted by the pathology panel in
the program as definite, probable or possible are included. Because of delays in definitive
diagnosis being received, incidence rates have been calculated up to end 1996 only, because
of the up to two year delay in notification experienced while awaiting confirmed
diagnosis and reconciliation with the state cancer registries. Figure 3.3 shows age-specific
incidence for males and females >20 years of age for the year 1996. Figures 3.4 and 3.5
show age-specific incidence trends over time for males and females. Figures 3.6–3.8 show
trends in world population >20 years of age standardised mesothelioma incidence by State,
sex and site for recent years
From 1 January 1980 to December 2000, a total of 5671 notifications had been received
by the program and register. Notifications show a continuing upward trend. The
Australian population has increased from 14.5 million in 1980 to 19 million in 2000. Mesothelioma
incidence rates, standardised to the world population >20 years have increased
from 11.8 per million per year in 1982 to 30 per million per year in 1996 (males and
females combined), 51.8 per million per year (male) and 5.9 per million per year (female).
The notifications prior to 1982 were probably the result of bedding in of a new program
and are artificially low (1980:16; 1981:104), although a smooth curve of increasing notification
rate starting from the early 1960s has since been demonstrated by retrospective
search (Figure 3.9 ). Between 1945 and 1979 there were 658 cases (535 male, 123 female)
in Australia
In 93.2% of all program cases the mesothelioma was pleural in site, 6.5% peritoneal
and only 0.3% of cases in other sites. Among men 94.3% were pleural, 5.3% peritoneal;
among women 86.3% pleural, 13.7% peritoneal. These proportions have been maintained
in register cases, with a slightly higher proportion of site not known being reported. The
female peritoneal proportion has dropped to 10.4%. Of the cases that underwent pathology
panel review, 96% were confirmed as mesothelioma (73% definite, 17% probable
and 6% possible). The most common occupational exposures were repair and maintenance
of asbestos materials (18%), shipbuilding (11%), asbestos cement production (7%),
asbestos cement use (7%), railways (6%), Wittenoom crocidolite mining/milling (6%),
insulation manufacture/installation (4%), wharf labouring (3%), power stations (3%),
boilermaking (2%), and para-occupational/hobby and environmental (15%). When the
earlier cases classed as ‘no history of exposure’ were reviewed it was found that 57 of the
203 so classified actually had history of some exposure recorded. Thus only around 18%
had no known history. Moreover, of this ‘no known history’ group, 81% had fibre counts
detected in the lungs, 30% with more than 106 fibre/g >2 micron including ‘long’ (>10
micron) fibres, suggesting that nearly all cases have been exposed. Indeed, absence of
fibres in the lungs does not negate exposure as fibres may have initiated mesothelioma
and then been cleared before deat
Conclusion
The high and increasing incidence of mesothelioma in Australia is due to high asbestos
use in the past, combined with poor hygiene practice, relatively high amphibole use in
asbestos cement products, slow recognition of chrysotile mesotheliomagenicity and excessive
focus on Wittenoom to the exclusion of other more common exposures. The expected
total number of cases from 1945 to 2020 is estimated to be about 18 000, based on models
by Berry55 and de Klerk et al.56 for Wittenoom, extrapolated for Australia as whole (assuming
Wittenoom contributes 5% of cases), and direct extrapolation from the best fit to the
empirical incidence curve, constrained to have a maximum value at 2010, following a 40-
year latency from the time of maximum exposure (1970) (Fig. 3.11). This will create a
heavy clinical and compensation load. The impact on non-occupationally exposed individuals
is another major issue.57 The various Australia State and Federal government authorities
are now developing a national strategy for dealing with this problem.
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