Occupational Medicine 2004;54:304–310
doi:10.1093/occmed/kqh073
IN-DEPTH REVIEW
Occupational respiratory disease in mining
M. H. Ross1,2 and J. Murray2,3
Abstract
This review is based on research-based literature on occupational lung disease in the
mining and related industries, focusing on conditions of public health importance
arising from asbestos, coal and silica exposure. Both ‘traditional’ and ‘new’ concerns
about occupational respiratory disease in miners are addressed, with the inclusion of
practical evidence-based findings relevant to practitioners working in developed and
developing countries. Mining is not a homogeneous industry since current miners
work in formal and informal operations with numerous, and often multiple,
air-borne exposures. A further occupational health challenge facing primary care
practitioners are ex-miners presenting with disease only after long latency. The
sequelae of silica exposure remain an occupational health priority, particularly for
practitioners who serve populations with concomitant HIV and tuberculosis
infection and even when exposure is apparently below the statutory occupational
exposure level. Coal workers’ pneumoconiosis, asbestos related diseases, lung cancer
and other occupational respiratory diseases remain of considerable importance even
after mining operations cease. While mining exposures contribute significantly to
lung disease, smoking is a major factor in the development of lung cancer and
chronic obstructive airways disease necessitating a comprehensive approach for
prevention and control of mining-related occupational lung disease.
Key words
Asbestos; coal; lung disease; mining; silica; smoking.
Received
13 February 2004
Revised
26 February 2004
Accepted
20 April 2004
occupational lung diseases are a function of the commodities mined, airborne hazard exposure levels, the period of
exposure and co-existing illnesses or environmental
conditions and lifestyle. The diseases and exposures
are too numerous to do justice to in a short review. Thus,
this review focuses on asbestos, coal and silica exposures
since these are the commodities of major public and
occupational health importance for occupational
practitioners serving ex and current mineworkers [1,2]
and are of considerable medico-legal significance. The
accent of the review is on recent research findings that
have implications for best clinical practice. This review is
based on recent comprehensive reviews of best practice
by South African physicians [1,2], classic undisputed
findings, research with which the authors are associated
and literature of the past 10 years, identified using Google
database search for the key words: mining occupational
lung disease with asbestos, coal, silica, smoking and
cancer.
Background
The relationship between mining and occupational lung
disease has been documented since the 1500s, when
Agricola described dust with corrosive qualities eating
away the lungs and implanting consumption in the body.
In the twenty-first century, this age-old relationship
between silica exposure and tuberculosis (TB) has
acquired a renewed importance with the growing
epidemic of HIV in developing countries, where the
informal or non-regulated mining sector is significant and
dust control less than optimal.
The relative prevalence and severity of mining-related
1
Mine Health and Safety Council, Johannesburg, South Africa.
2
School of Public Health, University of the Witwatersrand, Johannesburg, South
Africa.
3
National Institute for Occupational Health, Johannesburg, South Africa.
Correspondence to: M. H. Ross, School of Public Health, University of the
Witwatersrand, Johannesburg, South Africa. e-mail: [email protected]
Occupational Medicine, Vol. 54 No. 5
© Society of Occupational Medicine 2004; all rights reserved
304
M. H. ROSS AND J. MURRAY: OCCUPATIONAL RESPIRATORY DISEASE IN MINING 305
Asbestos
Producers and users of asbestos
Control and prevention of asbestos-related lung diseases
are recognized public health issues [3] and many
countries have either banned all types of asbestos or
severely restricted its use [4].
The mining and use of amphibole forms of asbestos
(primarily amosite and crocidolite) has ceased worldwide,
but chrysotile (the serpentine form) is still mined, e.g. in
Canada and Russia, and is utilized by many countries
(mainly African, Asian and South American) for, among
other things, water reticulation and housing. Chrysotileproducing countries have been strong protagonists for
chrysotile, and its unique properties, the lack of
inexpensive substitutes, plus the scientific evidence that it
is less harmful than the amphiboles [5] have prevented a
blanket international prohibition of chrysotile.
Sources of exposure
Given the widespread past use, potential sources for
asbestos exposure are many, even today [3]. Although the
number of miners still exposed to asbestos is minimal, the
manufacturing or removal of asbestos products, such as
ceiling boards, remains a hazard. People living in the
vicinity of asbestos mines, mills or manufacturing plants
may be exposed to the fibres environmentally. For
example, there is a high incidence of mesothelioma in
women who live or lived in the Quebec chrysotile mining
area [6] (the contamination of chrysotile, in this region,
by the amphibole tremolite, increases its toxicity).
Exposures from non-industrial sources have also been
documented in regions where the soil is contaminated
with asbestos fibres [7].
Presentation, diagnosis and clinical features
significant exposure to asbestos, as well as an increased
risk of developing mesothelioma (and possibly also lung
cancer) [10].
Asbestosis
As exposure levels in workplaces around the world are
increasingly meeting recommended control levels, the
rates of certification of death or disability from asbestosis
are falling in many countries [11]. However, asbestosis
deaths in the USA increased >10-fold from 1968 to 1999,
with no apparent levelling off of this trend [19].
Clinical diagnosis of asbestosis depends on establishing
the presence of pulmonary fibrosis with asbestos
exposure of sufficient intensity. The radiological features
of well-developed asbestosis seldom present a diagnostic
problem; interpretation of less marked changes is more
subjective, as ageing, smoking and chronic obstructive
pulmonary disease (COPD) can affect the specificity of
the chest radiograph. There is increased certainty when
rales and a low carbon monoxide diffusion capacity are
also present [13].
Although asbestosis is usually associated with
restrictive lung function, some patients exhibit a mixed or
obstructive lung function profile [14]. When radiological
or lung function changes are marginal, high resolution
computed tomography (HRCT) often shows parenchymal fibrosis and the presence of pleural plaques
provides additional evidence that the parenchymal
disease is asbestos related [15]. Asbestosis is not a risk
factor for TB [16].
Diagnosis of asbestosis for the purpose of legal
attributability calls for greater certainty and the use of
criteria that vary according to the relevant legal system.
At an international meeting in Helsinki in 1997, the
criteria for diagnosis and attribution of asbestos-related
diseases were reviewed and guidelines produced; in
addition to radiological studies, analysis of lung tissue for
asbestos fibres and bodies may be of assistance [17].
Pleural plaques
Malignant disease
Pleural plaques continue to be the most frequent, and
often only, manifestation of asbestos exposure and
asbestos exposure is the commonest cause of pleural
plaques. In the period 1992–1999, pleural plaques
(benign pleural disease) constituted 28–35% of occupational respiratory disease cases reported in the UK [8].
Pleural plaques, in the absence of parenchymal disease,
often do not cause signs and symptoms and are
commonly detected as an incidental finding on a routine
chest radiograph. In the past, pleural plaques were
labelled as ‘visiting cards’ for asbestos exposure, implying
that they had no impact on lung function. More recently,
however, pleural plaques have been associated with
respiratory disability [9]. A Swedish study showed that
pleural plaques on the chest radiograph indicated
The emergence of malignant asbestos-associated diseases
as important causes of death in asbestos-exposed
individuals can be attributed, in part, to workplace
controls, resulting in a decrease in the competing risk
from asbestosis and greater chance of survival into the
cancer age group.
Mesothelioma
In the UK, the number of mesotheliomas among males
increased almost 3-fold over the last 20 years, with 6475
cases in the 5 year period 1996–2000 [18]. In 1999, there
were 2500 deaths from mesothelioma in the USA, 20% of
which were in females and 15% in construction workers
[19]. Given the long incubation period of mesothelioma
306 OCCUPATIONAL MEDICINE
(20–40 years), one can realistically expect cases to
continue to present well into the twenty-first century [3].
Although in the UK it has been estimated that the
mesothelioma rates would decline by only the second
decade of the twenty-first century [20], there is some
evidence [21,22] that the rates may be dropping already.
Despite many years of clinical research, there is still no
effective therapy for malignant mesothelioma; untreated
the median survival time is 9 months. Chemotherapy,
radiotherapy and surgery have not shown consistent
improvements in survival [23].
Lung cancer
The association of lung cancer with asbestos exposure is
well known. There is currently debate about whether
asbestos exposure in itself is a cause of increased lung
cancer risk, or whether it is through the development of
asbestosis in association with asbestos exposure [24,25],
as most people believe.
Smoking, asbestos exposure and prevention of lung disease
The risk of lung cancer in asbestos exposed individuals is
greatly enhanced by cigarette smoking, but the
multiplicative model has recently been challenged [26].
Other factors influencing the risk of lung cancer in
exposed workers include intensity of exposure and fibre
type. Fibre length may or may not play a role in the
pathogenesis [27].
Pathologic studies do not show evidence of an
association between asbestosis grade and smoking,
although there is evidence to suggest that smoking
enhances the retention of fibres in the lungs [28]. Both
the possible role of smoking in the initiation and
progression of fibrotic parenchymal disease and its
established role in increasing the risk of lung cancer are
strong indications for anti-smoking advice to be given to
asbestos-exposed individuals and for instituting smoking
cessation programmes in workplaces contaminated by
asbestos dust.
Coal workers’ pneumoconiosis
Occupations at risk
There has been a steady decrease in the numbers of coal
miners in Western Europe and the USA. However, the
mining industry in these countries still employs large
numbers (~200 000 in the USA) [29], as in Eastern
Europe, India, China, Africa, Australia and South
America. As the number of miners has decreased,
however, mechanization has increased potential dust
exposure. Hence, former and current coal workers are
likely to develop coal workers’ pneumoconiosis (CWP)
for the foreseeable future.
During the last 30 years, the prevalence of CWP
has fallen consistently in the USA. In active underground miners included in the National Institute for
Occupational Safety and Health (NIOSH) Coal Workers’
X-ray Surveillance Program [19], rates fell from >10% in
the early 1970s to <2% in the late 1990s (consistent with
the estimated current rate in South Africa of 2.6%) [30].
Similar trends have been noted in Europe [3,8].
Nevertheless, dust levels in coal mines are still high. A
quarter of coal mine dust exposures recorded by Mine
Safety and Health Administration (MSHA) in the USA
exceeded the NIOSH recommended exposure limit
(REL) of 1 mg/m3 [19]. The permissible exposure limit
(PEL) for respirable coal dust is 2 mg/m3 in the USA.
However, since new cases are occurring even among
miners who have worked exclusively under current dust
exposure limits, an evaluation of the dust levels in mines
where these workers were employed is underway [31].
In addition to coal mining per se, other occupations at
risk include coal trimming (which involves loading and
stowing coal in stores or ships’ holds) and the mining and
milling of graphite.
Risk and prevalence
Fibrosis associated with coal dust exposure is
considerably less intense and extensive than that evoked
by the more bioactive dusts, such as silica and asbestos
[32]. The risk for CWP depends on the total dust burden
in the lungs and is also related to the coal rank, which is
based on its carbon content (anthracite has a higher rank
than bituminous, followed by sub-bituminous and
lignite) [33]. In the higher ranking coal, there may be a
greater relative surface area of the coal dust particles,
higher surface-free radicals and higher silica content [34].
Silica exposure and hence silicosis is more common in
mines with a high grade of coal [35] and in workers such
as roof bolters who work outside of the coal seams in
quartz-containing rock [36].
Both the presence and stage of CWP, and the
development of progressive massive fibrosis (PMF),
appear to be related to the intensity of dust exposure, age
[34], proportion of inhaled silica in the dust and its
surface bioactivity, individual immunological factors, and
the presence of tuberculosis.
Presentation, diagnosis and clinical features
For many years, simple CWP was regarded as a disease
without symptoms or physical signs. However, current
evidence shows that coal mining, even in the absence of
CWP and controlling for smoking, is associated with
chronic bronchitis, chronic airflow limitation and
emphysema [33,37]. In their comprehensive review,
Coggon and Newman Taylor [38] concluded that:
M. H. ROSS AND J. MURRAY: OCCUPATIONAL RESPIRATORY DISEASE IN MINING 307
the balance of evidence points overwhelmingly to coal
· mine
dust being a cause of impaired lung function;
this
can
be disabling;
· the best estimate
the loss of FEV (forced expiratory
· volume in 1 s) in ofrelation
to exposure of coal miners is
1
·
0.76 ml/g h/m3; and
the combined effects of coal mine dust and smoking on
FEV1 appear to be additive.
Symptoms of cough and sputum reported by most coal
miners are likely to be a consequence of dust-induced
chronic bronchitis. Breathlessness on effort is usually
caused by associated chronic airflow limitation or by the
development of PMF [33]. Respiratory impairment and
disability increase as PMF progresses.
The chest radiograph remains a cornerstone of the
diagnosis of CWP. However, because it is insensitive to
the presence of macules and nodules [39], CT (computed
tomography) may be more useful in individual cases.
Most evidence suggests that coal mining is associated
with a decreased risk of lung cancer, but an increased risk
of stomach cancer [40]. CWP alone does not carry an
increased risk for mycobacterial infection, either by
Mycobacterium tuberculosis or nontuberculous mycobacteria (NTM), but treatment of latent tuberculosis
infection should be considered for coal workers who are
thought to have had significant silica-dust exposure or
who have evidence of silicosis [41]. The adverse
respiratory effects of CWP and tobacco exposure
necessitate active smoking cessation counselling for
exposed individuals.
suggested that the level be lowered to 0.01 mg/m3
[46,47].
Although the major determinant of silicosis is the lung
dust burden, there is accumulating evidence that other
variables such as freshly fractured silica, admixtures of
other minerals, e.g. clay components which can coat the
surface of the silica [29] and peak exposures also may be
important [36]. Individual susceptibility to the disease
determined using biomarkers may also play a role [48].
Diseases associated with silica exposure
An excellent review by Mossman and Churg [49]
summarizes the processes whereby silica produces
inflammation and fibrogenesis in the lung. Although
silicosis continues to be the most common disease
associated with silica exposure, the recent scientific
literature has drawn attention to other silica-associated
diseases.
Lung cancer
Recent authoritative reviews concluded that there were
sufficient data to support an association between silicosis
and lung cancer [12,42,47]. However, there remains
debate about whether silica exposure, in the absence of
silicosis, carries an increased risk for lung cancer
[42,47,50]. The cancer risk may also be increased by
smoking and exposure to other carcinogens, such as
diesel products and radon, in the work place [51].
Tuberculosis
Silicosis
Risk and prevalence
Silicosis continues to be a major disease world wide, even
in developed countries, affecting workers in mining and
other occupations, including construction and foundries
[3,19]. This avoidable disease remains a significant cause
of morbidity and mortality [42]. Furthermore, reported
cases are a gross underestimate of the total cases of
silicosis [43], and in some settings, the prevalence of
silicosis is rising [44].
Although silica dust is one of the most documented
workplace exposures, there is controversy over the precise
quantitative relationship between dust inhalation and the
development of disease. Scientific evidence is increasingly
demonstrating that exposure over a working lifetime to
the commonly used standard of 0.1 mg/mg3 will result in
a significant burden of radiological silicosis and also
death from silicosis and lung cancer [45]. The evidence is
insufficient to indicate whether or not halving this level to
0.05 mg/m3 would be protective and hence it has been
The association between silicosis and tuberculosis has
long been recognized. Rates for active tuberculosis in
silicotic subjects range from 2- to 30-fold more than those
in the same workforce without silicosis [52]. Factors
which influence the development of tuberculosis include
the severity of silicosis, the prevalence of tuberculosis in
the population from which the work force was drawn, as
well as their age, general health and HIV status [2,52].
Exposure to silica, without silicosis, may also predispose
individuals to tuberculosis [52,53]. Although M.
tuberculosis is the usual organism, NTM account for a
large proportion of the mycobacterial disease in some
populations [42,54]. The prevalence of HIV infection in
developing countries has and will increase the burden of
tuberculosis in miners exposed to silica dust. A recent
study [55] of the effect of HIV infection on silicosis and
tuberculosis incidence in black South African gold
mineworkers found that HIV infection increased the
incidence of tuberculosis by five times and silicosis
increased the incidence of tuberculosis by three times.
The co-existence of HIV and silicosis increased the
incidence of tuberculosis multiplicatively by fifteen times.
308 OCCUPATIONAL MEDICINE
Connective tissue diseases and renal disease
Associations have been reported between exposure to
silica and certain connective tissue diseases including
progressive systemic sclerosis, systemic lupus erythematosis, rheumatoid arthritis, and renal disease [12,56].
Chronic obstructive airways disease
Chronic obstructive airways disease (emphysema) and
chronic bronchitis are common manifestations of long
term occupational exposure to silica dust and can develop
in silica-exposed individuals with or without radiological
signs of silicosis. In their comprehensive review, Hnidzo
and Vallyathan [57] provide evidence that smoking can
potentiate the effect of silica dust on airflow obstruction.
Presentation, diagnosis and clinical features
Silicosis is diagnosed on the basis of a history of exposure
and the characteristic radiographic changes. Occasionally,
however, even advanced silicosis (diagnosed by histology)
may not be recognized on a chest radiograph [43]. It also
remains unclear whether smoking predisposes exposed
miners to silicosis or nonspecific radiographic changes
from smoking are misinterpreted as silicosis [58].5
People with silicosis are usually asymptomatic. The
appearance of breathlessness is usually associated with a
complication such as progressive massive fibrosis or
tuberculosis, or may reflect associated airway disease.
Cough and sputum production are common symptoms
and usually relate to chronic bronchitis but may reflect
the development of tuberculosis or lung cancer. The
presence of cough, haemoptysis, weight loss, fever or any
new radiographic feature should be pursued with culture
of sputum or bronchoalveolar lavage fluid or with culture
and histological examination of tissue. It should be noted
that those with silicosis are also at risk for extrapulmonary tuberculosis [42,52].
Treatment and prevention
There is currently interest in the use of therapeutic agents
to treat silicosis and in lung lavage to remove silica from
the lung but a favourable impact on progression of acute
or chronic silicosis has not been demonstrated [59].
Management of all forms of silicosis should also be
directed toward control of mycobacterial disease. All
subjects with silicosis should have a tuberculin skin test
and, if it is positive, be offered treatment for latent
tuberculosis infection [41].
The adverse effects of smoking and the interaction
between silica exposure and smoking in the development
of COPD, make smoking cessation programmes
particularly important for silica-exposed miners [56,57].
M. H. ROSS AND J. MURRAY: OCCUPATIONAL RESPIRATORY DISEASE IN MINING 309
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