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| Journal of the New Zealand Medical Association,
05-November-2004, Vol 117 No 1205
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Mortality, morbidity, and asbestosis in New Zealand: the
hidden legacy of asbestos exposure
Pamela Smartt
Asbestosis is a diffuse fibrotic lung disease resulting from
the inhalation of asbestos fibres.1 High fibre
doses (25–100 fibre/ml/yr)2 are generally
required to produce clinically significant asbestosis within an
individuals’ lifetime3,4 with milder
fibrosis at lower dose levels.5 Asbestosis is
thus a marker of high asbestos exposure in individuals and its prevalence a
potential indicator of high exposure in populations.
Asbestosis was the first disease to be attributed to
asbestos exposure in the workplace,6 80 years
later it is still a serious public health issue in industrialised
countries.7 Not only is asbestosis a grossly
debilitating, irreversible, and progressive
disease,8 individuals who are afflicted have a
greatly increased risk of an number of diseases including lung cancer, cancers
of the digestive system, and non-malignant respiratory
disease.9–12
National mortality and morbidity statistics underestimate
the public health impact of asbestosis as they report the primary cause of death
(COD) or primary diagnosis, which may not indicate or identify the underlying
disability.13,14 This is particularly
concerning as the National Asbestos Registers suggest that asbestosis is more
widespread than malignant asbestos disease in New
Zealand.15 Predictions of the scale of the
asbestos disease epidemic have been modelled on mesothelioma
data;16–18 the contribution of
non-malignant disease such as asbestosis has been largely ignored. With a
latency period inversely proportional to exposure
level,2 but generally reported as 15–30
years19,20 the health burden of asbestosis
should peak earlier than mesothelioma thus potentially providing useful
additional information about the size and extent of the current epidemic of
asbestos diseases.
In this study, the recorded health events of individuals
diagnosed with asbestosis in New Zealand between 1974–2001 are examined.
The purpose of the study is to highlight the public health importance of
asbestosis and assess the overall health impact of this disease in New Zealand.
Mortality, cancer, and hospital records of New Zealand men
diagnosed with asbestosis are examined to determine:
The
potential contribution of morbidity data to existing models of the asbestos
epidemic is also discussed.
MethodsNational
mortality records—All individual death, cancer, and
hospital-discharge records that were available at the time of study were
obtained on CD-ROM from New Zealand Health Information Service (NZHIS). These
data comprised 690,198 death records covering a period from 1974–1999;
266,121 cancer records covering a period from 1980–1998; and 327,940
public and private hospital-discharge records covering a period from
1994–2001.
All records were supplied without identifying
information as annual records in discrete Microsoft Excel or Borland dBASE IV.
Individual death records with asbestosis (ICD-9 code 501) or lung cancer (ICD-9
code 162) anywhere in the death record were extracted from the mortality files.
All hospital discharge records for patients with a
diagnosis of asbestosis in any of five diagnosis fields were extracted from the
public and private hospital files. Two new databases were constructed from these
files using an INFORMIX database; one comprising all relevant mortality records
(n=24,590), and another comprising all relevant hospital discharges for male
patients with asbestosis (n=706).
Database
linkage—Individual death and hospital discharge records in each of
the two main databases were linked separately via the unique encrypted
healthcare user (ENC_HCU) number to the cancer registration database. All
matching ENC_HCU records were crosschecked against sex and date of birth to
minimise the chances of case mismatch.
Time
series—All data were not available for all periods. Limitations
were imposed by the availability of verified database records, ENC_HCU number
for cross-referencing and relevant occupation codes. Three times series had the
required characteristics:
Where required, the mortality and hospital
discharge datasets were linked via their unique ENC_HCU number to each other and
to New Zealand Cancer Registry records for 1980–1998. These series
determined the overall structure of the study.
Mortality
rates—Age standardised mortality rates were calculated using
estimated population data obtained from HZHIS publications for the relevant
years. For comparative purposes, all rates were standardised to the Segi World
population.
Asbestos
registers—The National Asbestos Registers were set up in 1991 upon
the recommendation of the Asbestos Advisory
Committee21 to register people who had had
‘significant exposure’ to asbestos. The National Asbestos Medical
Panel reviewed cases referred via a notifiable occupational disease (NODs) card
or a doctor’s letter. The number of cases registered between March
1992–July 1998 was obtained from the 1997–1998
report15 supplemented by figures for individual
years obtained directly from OSH. The ACC Scheme Reporting and Forecasting Unit
supplied figures for the number of claims for all ‘inhalation
diseases’ by sex and year between 1992–1998.
ResultsMortality
trends (1974–1999)—316 New Zealand males died with asbestosis
between 1974–1999. During the same period, 24,590 male deaths were
associated with lung cancer; 90 (0.4%) of these record asbestos exposure or
asbestosis in the death record. While male lung cancer declined from 1983,
asbestos-related deaths generally increased over the period, rising from 2
deaths in 1977 to 40 deaths in 1999. For lung cancer deaths associated with
asbestosis, annual numbers were small and fluctuating but there was a
discernible trend in numbers with averages of 0.5, 2.1 and 6.6 cases per year in
the 1970s, 80s, and 90s respectively.
The number of males dying with asbestosis increased steeply
in the 1990s. This increase was still apparent when pleural cancer (used as a
surrogate for mesothelioma) deaths were removed. Age-standardised mortality
rates revealed similar trends with a more pronounced downward trend for lung
cancer (Figure 1).
Cause of death
(COD)—In the period 1988–1999, 264 asbestos associated male
deaths were recorded. The majority (86%) were European; the median age for the
whole group was 71 years (35–92 years). The contribution of asbestosis to
the COD is shown in Table 1.
Table 1. The contribution of asbestosis to the deaths
of 264 New Zealand males registered between 1988–1999.
*As
coded in the national mortality data sets; †Cause of death (COD) indicated
by the death certificate.
Only 44 (17%) of deaths were attributed directly to
asbestosis—ie, asbestos was recorded as the ‘underlying’ COD.
In the remaining cases (n=220, 83%), asbestos was recorded as a
‘contributing’ COD. The primary COD for these 220 decedents is shown
in Table 2.
Table 2. The primary cause of death for 220 New Zealand
males dying with asbestosis recorded as a contributing cause of death between
1988–1999
Seventy-three percent of deaths were attributed to cancer
with a further 11% attributed to ‘other disease of the respiratory
system’ including cases which may have been undiagnosed asbestosis.
Circulatory disease accounted for only 12% of all deaths. The primary organ
systems involved with malignant and non-malignant disease are shown in Table
3.
Table 3. Primary disease sites for New Zealand males
dying with asbestosis 1988–1999
*Includes
one cancer of other and ill-defined sites with asbestosis and
mesothelioma.
Most (75%) patients died of malignant (64%) or non-malignant
(11%) respiratory disease including:
In addition, 14 patients of the males died from
circulatory diseases including ischaemic heart disease (63%), cerebrovascular
disease (19%), diseases of the arteries (11%), and endocardium disease (7%).
Nine patients died from digestive disease: seven (3%) were digestive cancers
including neoplasms of the oesophagus (n=1), stomach (n=1), colon (n=2),
peritoneum (n=2), and ill-defined site (n=1).
Overall, cancer was the primary cause of death in men dying
with asbestosis between 1988-1999. The median age of death for those with cancer
was lower than those without (69 and 74 years). Finally, out of a total of 264
deaths 209 (79%) were attributed directly to diseases of the airways with a
further five deaths attributed to cancers of ill or undefined sites likely to
have been cancers of the respiratory system.
Occupation—The
decedent’s last occupation, as recorded on the death certificate, was
available for deaths between 1988–1997. Three years were not available due
either to known errors in the coding (1991) or coding discontinuity (1998,1999).
189 men dying with asbestosis during the study period were classified to 23
sub-major occupation classes (NZSCO90). One death was not classified.
In each occupational class, the number of deaths that could
be attributed primarily to asbestosis, pulmonary fibrosis, pleural, lung or
peritoneal cancer was determined (Figure 2). Trades workers (building, metal,
and machinery) accounted for 76 (40%) of the deaths; professional and associated
occupations accounted for a further 26 (14%) of the deaths.
Plant and machine operators also accounted for 26 (14%)
deaths while labourers accounted for 15 (8%), workers with unclassifiable
occupations 15 (8%), and corporate managers (including quarry and construction
managers) 11 (6%) of all deaths, respectively
The remaining 19 (10%) deaths were distributed between seven
occupational groups spanning clerks, technicians, service and sales workers,
agricultural and fishery workers, and armed forces. Interestingly, 86% of deaths
in physical science and engineering associate professionals were attributed
primarily to pleural cancer while 70% of deaths amongst industrial plant
operators were attributed to asbestosis, peritoneal or lung cancer—all
indicators of high asbestos exposure.
Building trade workers had the highest number of deaths
attributed primarily to pleural cancer (17/47), lung cancer (15/47), and
asbestosis (5/47).
Morbidity—Credible
hospital discharge records were only available from 1994 (NZHIS personal
communication). During this period, there were 706 hospital discharges involving
539 patients. Most individuals were only hospitalised once during the period,
however a significant number (n=123) of patients averaged three (range
2–11) hospitalisations during the period (1994–2001).
The majority of hospitalisations (n=450, 64%) were coded as
acute admissions, 120 (17%) were arranged admissions, 113 (16%) waiting list,
and 13 (2%) ACC-related. Over the whole period, not counting 97-day cases,
patients were in hospital for an average of 7 days (total 4,319 days, median 5
days). The main reasons for hospitalisation, as indicated by the primary
diagnosis, are shown in Table 4.
Table 4. Primary diagnosis for 706 hospital discharges
for New Zealand males with asbestosis in the period 1994–2001.
In most cases (n=507; 72%), patients were admitted to
hospital for treatment of respiratory disease (41%), circulatory disease (19%),
or neoplasms (11%).
Basic hospital costs (excluding drugs) for ninety discharges
recorded in 2001 are shown in Table 5.
Table 5. Hospital costs for 69 male New Zealand
patients with asbestosis in 2001
*Diagnostic
Related Groups
Half of the estimated cost of hospital discharges can be
attributed directly to respiratory disease ($172,725)—with a tracheostomy,
interstitial lung disease, chronic obstructive disease, and respiratory
infections and inflammation accounting for 89% of this cost.
The temporal pattern of these discharges is shown in Figure
3 for 706 discharges involving 539 patients. Discharges rose steeply from 1994,
peaked in 1999 and decreased successively in 2000 and 2001.
The National Asbestos
Registers and Accident Compensation Corporation (ACC)
claims—Between March 1992–July 1998, 136 males (mean age of
approximately 66 years) were registered with asbestosis, the majority (80%)
were, or had been, smokers. Approximately 25% were likely to have had high
exposure to asbestos (ie, asbestos processors, asbestos sprayers, and
watersiders handling raw asbestos).
Most of the reminder were employed in secondary industries
and included plumbers, fitters, laggers, carpenters, and builders. The mean
latency period was reported as 39 years (range 15–71 years). In contrast
to all other sources, the National Asbestos Register recorded numbers falling
sharply from 1992–1998. Registered ACC claims for the period could only be
retrieved for all ‘inhalation diseases – Asbestos/Lead’
(personal communication).
Overall, during the period 1992–1998, 1705 claims were
made by New Zealand males. The ACC Workwise Asbestos Claim Database recorded 78
claims in 1997, 42 (54%) claims were successful including 6 (14%) for
asbestosis, 33 (79%) for mesothelioma, and 2 (5%) for lung cancer.
DiscussionIt has been estimated that
20%–40% of all adult men are likely to have some past occupation that may
have exposed them to asbestos in the
workplace.5 In New Zealand, over 8,000 men were
directly employed in the asbestos industry (Report of the Asbestos Advisory
Committee 1991) with at least a further 1500 men estimated to have been exposed
in ‘downstream’(ie, secondary)
industries.22–24
Before 1940, virtually all asbestos products were imported
into New Zealand. Thereafter, raw asbestos was also imported and manufactured
into asbestos-containing products (mainly cladding and pipes). Imports of raw
asbestos peaked at around 12,500 tonnes in
1974.18
The import of raw amphibole (blue and brown) asbestos into
New Zealand was banned in 1984; chrysotile (white) asbestos was banned in 2002.
Workforce regulations to protect employees were not drafted until 1978—in
1983, employers were obliged to inform workers of the particular dangers of
smoking in asbestos workers. In New Zealand, asbestos exposure in the working
population was probably highest between the 1940s–1980s. The legacy of
this exposure is an ageing population of men with asbestos-related disease,
which includes some of the most debilitating malignant and non-malignant
diseases of the lung.
The unfolding New Zealand mesothelioma epidemic was
described by Kjellstrom and Smartt,18 however
the full health impact of occupational asbestos exposure is likely to be much
greater. In this study, an increasing trend in non-malignant disease similar to
that reported elsewhere13 is documented.
Official mortality statistics compiled from the primary COD
are known to underestimate the health impact of
asbestosis.10,11,13,14 This is supported in the
present study, with only 17% of asbestosis-related deaths being reported in the
published mortality tables (Table 2).25
Of the remaining 220 (83%) deaths, cancer (particularly
cancer of the respiratory tract) was sited as the primary COD. Indeed, the
increased risk of cancer in individuals with asbestosis has been widely
reported, with lung/pleural and gastrointestinal cancers
predominating.9–12 In the present study,
the primary cause of death for a high proportion (29%) of 264 patients dying
with asbestosis was pleural cancer (with a further 23% attributed to lung
cancer).
It has been estimated that between 6%–23% of lung
cancer deaths could be attributable to asbestos exposure in the
workplace.26–28 In this study, only a
very small proportion (0.4%) of individuals dying with lung cancer had any
mention of asbestos exposure or asbestosis in the death record. While this
proportion peaked at 0.7% (n=12) in 1997, it is still far short of the minimum
expected 6% (n=56) cases predicted by some
studies,26,27 or the minimum of 74 cases
suggested by Kellstrom and Smartt.18
ACC claims and the National Asbestos Register similarly
under-represent lung cancer cases in New Zealand as
elsewhere.14,26 Since increases in the number
of asbestos-related lung-cancer deaths are predicted to occur at a time when
male lung cancer deaths overall are decreasing (Figure 1), the proportion of
asbestos-related lung-cancer deaths may be greater than predicted. Thus, more
active attempts to diagnose asbestosis and determine likelihood of asbestos
exposure in the current male population, particularly those who have been
smokers or who have lung cancer, is warranted.
Under-reporting of asbestos-related lung cancer mortality
has been attributed to possible lack of awareness of exposure and the
possibility that workers may not remember casual exposure 20–40 years
earlier. However, the most likely reason that asbestos-related lung cancer
deaths are under-reported is the very high prevalence of smoking (80%–85%)
in the occupations most likely to be exposed to asbestos in the workplace and an
assumption that lung cancer in smokers is most likely to be causally related to
tobacco.29
This finding is particularly disturbing, as it has been
shown that the likelihood of lung cancer in asbestos-exposed workers who also
smoke is 5 times greater than the likelihood of lung cancer in smokers not
occupationally exposed to asbestos, and 10 times greater than for non-smoking
asbestos workers (seminal work of Selikoff reported in Frank
1979).30
Eighty percent of men registered with asbestosis on the
national register were smokers or ex-smokers. Smoking and asbestosis has been
less studied than smoking and asbestos-induced lung cancer. However, it is known
that smoking inhibits airways clearance of fibres, contributes to the severity
of asbestosis, and (in patients with progressing asbestosis) is a significant
predictor of lung cancer.31–34 The main
point here is that, in smokers, asbestos exposure cannot be ignored because of
the hugely magnified risk of lung cancer.
Indeed, in many current and ex-smokers, a clinical diagnosis
of asbestosis may be the first indication of this increased risk. Immediate
cessation of smoking, prompt treatment for respiratory infections, and regular
screening for lung cancer and related malignancies is considered essential in
all cases of asbestosis.35
The effect of past exposure to asbestos on workers in the
secondary (or ‘downstream’) asbestos industries such as
construction, shipbuilding, automobile, and railway repair workers has been
widely reported and summarised for chrysotile asbestos by the World Health
Organization.36 It has been argued that such
exposures have often been overlooked37
particularly if employment was of short duration. However, in terms of
health effects, there is no threshold for asbestos exposure, and a strong dose
dependency has been demonstrated;36,38 both
long-term low-exposure and short-term high-exposure may result in serious lung
disease such as asbestosis.2,39,40
In this study, 23 different occupational groups were
recorded in the death certificates of men dying with asbestosis in New Zealand
(Figure 2). The prevalence of asbestos-related disease (indicated by the last
known occupation) was highest in New Zealand trades workers, plant and machine
operators, labourers, and casual workers—a picture confirmed in the
National Asbestos Registers Reports and studies in Europe and
America.14–16,35,41,42 However the data
reported here also suggest that some parts of the workforce in all major
occupational groups may have had some level of past exposure to
asbestos.
Most work highlighting the health impact of asbestos has
arisen from the reporting of mortality data; however, morbidity and
quality-of-life issues are also an important part of the impact of asbestos on
population health. In this study, the burden of hospital care of patients with
asbestosis is examined to highlight this issue. Asbestosis sufferers have a
large number of acute hospital admissions resulting, for many, in substantial
(5–7days) episodes of care. Most are hospitalised with respiratory
problems (Table 4) often requiring costly interventions for conditions such as
interstitial and chronic obstructive lung disease, respiratory infections, and
inflammation.
Interestingly, during a period when lung cancer in males
overall has been declining, hospitalisation for patients who have asbestosis has
steadily and substantially increased. In these patients, hospitalisations peaked
in 1999, then declining progressively through 2000 and 2001 (Figure 3). This
decline may be short-lived; however, if it continues, it may contribute
significantly to the accumulating information on the scale and timing of the
asbestos disease epidemic. Indeed, hospitalisation rates may be used to estimate
the prevalence of asbestosis; information that is difficult to obtain from other
sources.
Predictions of the scale of the asbestos epidemic have been
modelled using mesothelioma data; however since the average latency period for
the development of asbestosis is reported to be approximately 10 years shorter
than for mesothelioma, trends in health events relating to asbestosis may be
expected to provide the first evidence that the asbestos epidemic is peaking.
There are a number of well-known limitations in a study of
this type.41 Inaccuracies are known to occur in
the information obtained from death certificates. Causes of death can be
misclassified because of confounding factors (such as smoking), other
occupational exposures, and comorbidities contributing to the under-recognition
of asbestos-related mortality. This is often exacerbated further by uncertainty
relating to diagnostic criteria for asbestosis and differential diagnoses of
idiopathic pulmonary fibrosis or congestive heart
failure.8
Occupation recorded in the death record only relates to the
last full-time occupation, and may not be an accurate or fair indication of
asbestos exposure. However, the occupations highlighted in this study are the
same as those highlighted in cohort studies suggesting that the overall picture
obtained from these records may have some general validity. Finally,
improvements in the diagnosis of asbestosis, raised awareness, and improvements
in data collection have undoubtedly contributed to increase trends reported in
this study; however, with the exception of asbestos-related lung cancers, the
changes observed are too great to be explained in terms of these factors alone.
The bulk of the reported worldwide evidence suggests that
occupational diseases (including asbestosis) are under-diagnosed and
under-reported22,43,44 and that reported cases
are ‘just the tip of the asbestos diseases iceberg’.
Author information:
Pamela Smartt, Senior Research Fellow, New Zealand Health Technology Assessment
(NZHTA), Department of Public Health and General Practice, Christchurch School
of Medicine, Christchurch
Acknowledgements:
Most of this work was undertaken while the author was employed as a Senior
Research Fellow with the HRC-funded New Zealand Environmental and Occupational
Health Research Unit, Division of Community Health, University of Auckland.
I thank Professor Tord Kjellstrom (for his interest in this
work and comments on earlier drafts); Chris Lewis, Senior Information Analyst,
New Zealand Health Information Service (for his support in supplying anonymous
mortality, cancer registration and hospital discharge records); and Roger
Marshall, Senior Lecturer in Epidemiology and Biostatistics, School of
Population Health, University of Auckland (for critiqueing the paper and
provided helpful comments).
Correspondence: Dr
Pam Smartt, Senior Research Fellow, New Zealand Health Technology Assessment
(NZHTA), Department of Public Health & General Practice, Christchurch School
of Medicine, PO Box 4345, Christchurch. Fax: (03) 364 1152; email: pamela.smartt@chmeds.ac.nz
References:
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