Download Working with asbestos and the possible health risks

Occupational Medicine 2015;65:6–14
doi:10.1093/occmed/kqu175
In-depth review
Working with asbestos and the possible health risks
D. Sen
Centre for Occupational and Environmental Health, University of Manchester, Manchester M13 9PL, UK.
Correspondence to: D. Sen, Centre for Occupational and Environmental Health, University of Manchester, Oxford Road,
Manchester M13 9PL, UK. E-mail: [email protected]
Background The generic term asbestos refers to a group of crystalline mineral silicates that occur naturally in
various forms. Because of their properties of strength, heat and electrical resistance and their ability
to withstand corrosion by acids and sea water, asbestos was used extensively both in the UK and
worldwide.
Aims
To provide a historical perspective of this ubiquitous occupational hazard, consider the key changes
in UK legislation aimed at improving the management of this occupational health risk and describe
the evidence from the scientific literature concerning asbestos and disease.
Methods
Original articles, reviews (including reference textbooks) and scientific literature in PubMed and
other principal medical science databases, 1960–2014, were searched. Publications by regulatory
agencies and by governmental organizations were also considered and included where relevant.
Results
Asbestos remains the biggest cause of cancer deaths worldwide. For malignant mesothelioma deaths
alone, it is estimated that in the UK, between 2015 and 2020, the number of cases will peak at 2500
cases annually. It is not clear whether there is a safe level of asbestos fibres in air. Evidence for the
efficacy of health surveillance is lacking.
Conclusions Although the use of asbestos was banned in the UK in 1985 (amosite and crocidolite) and 1999
(chrysotile), it remains a significant occupational risk factor for work-related morbidity and mortality, causing both benign and malignant diseases, often with long latency. Further research is needed
regarding exposure levels and health surveillance.
Key words
Asbestos; asbestosis; long latency; lung cancer; mesothelioma; screening.
Introduction
Asbestos is a generic term for a group of crystalline mineral silicates that occur naturally in various forms. They
result when siliceous minerals are leached out of rock by
water and then re-crystallize in spaces within the parent rock as compound metallic silicates. There are various morphological types that differ in their mechanical,
chemical and toxicological properties [1–3]. Table 1 lists
those that come under the term ‘asbestos’ as defined in
Regulation 2 of The Control of Asbestos Regulations
2012 [4]. Any mixture that contains one or more of these
fibres at more than trace amounts is within the definition. Debris containing asbestos is also covered by asbestos legislation [4].
Asbestos is resistant to heat and other means of
destruction. Its fibrous nature enables it to be woven into
cloth, incorporated into cement materials, ceiling tiles,
brake and clutch linings, flooring, resins, polymers and
© Crown copyright 2015
filter papers. In the 19th and 20th centuries, asbestos was
regarded as safe and widely used in a large number of
industries with minimal control of exposure. From 1950
to 1985, it was extensively used in construction and ship
building for insulation and fire protection and for friction
materials and filters. Any building constructed during this
period is likely to contain some type of asbestos-containing material, which is possibly the most important cause
of inadvertent exposure to asbestos. In the UK, asbestos
of any kind has not been used in manufacturing since
1999 but may be found (managed or removed), sometimes accidentally, during other work activities in connection with repair and maintenance or refurbishment.
Historically, the three main types of asbestos commonly used in industry were:
•• chrysotile, commonly
known as ‘white asbestos’,
and consisting of bundles of soft, flexible fibres
several centimetres long, serpentine (morpholo­
gically curved) fibres;
D. Sen: Asbestos Workers and Their Risks 7
Table 1. Morphological types defined as ‘asbestos’ in Regulation
2 of The Control of Asbestos Regulations 2012
Asbestos actinolite
Asbestos grunerite (amosite)
Asbestos anthophyllite
Chrysotile
Crocidolite
Asbestos tremolite
CAS No. 77536-66-4
CAS No. 12172-73-5
CAS No. 77536-67-5
CAS No. 12001-29-5
CAS No. 12001-28-4
CAS No. 77536-68-6
•• crocidolite,
commonly known as ‘blue asbestos’,
consisting of shorter, stiffer, straight fibres;
•• amosite, commonly known as ‘brown asbestos’
and consisting of coarse, straight fibres of iron
magnesium silicate.
As a naturally occurring fibrous mineral, asbestos is generally grouped into two classes, which differ significantly
in terms of their physical and chemical properties. The
serpentine class, which includes chrysotile asbestos, are
more easily cleared by mucociliary action and broken
down. The amphibole class, which includes amosite, crocidolite, tremolite, actinolite and anthophyllite asbestos,
are more resistant to clearance from the body, with a
longer residence time [5]. Of the three types most commonly used, and now found in construction work (chrysotile, amosite and crocidolite), all cause severe health
effects, although amosite and crocidolite fibres are recognized as being more dangerous to health than chrysotile
[1,6].
All people who have worked with asbestos are potentially at risk of developing asbestos-related lung disease. Health effects characteristically take many years to
develop and people exposed to asbestos often develop
lung disease in later life, including in retirement, due to
exposure many years previously. Asbestos is currently
classified by the International Agency for Research on
Cancer (IARC) as a group 1 (‘definite’) human carcinogen [7].
Historical perspective
One of the first suggestions that exposure to asbestos
could cause lung disease was at an industrial disease
board enquiry in 1899. Cases of lung fibrosis were recognized as being associated with asbestos in the early 20th
century, soon after the start of mining and exploitation of
the mineral ore on an industrial scale, but were masked
by the high incidence of tuberculosis. In the early 1950s,
epidemiological evidence identified an increased risk of
lung cancer from exposure to asbestos in the British textile industry and the risk to shipyard workers was also
recognized [1,8]. By the end of the 1960s, a case–control study in South African miners showed an association with mesothelioma and asbestos exposure [9]. It was
also shown that the excess of lung cancer that occurred
in many cases of exposure to asbestos fibres reflected
an interactive effect of asbestos and tobacco smoking
[1,8,10].
The Asbestos Survey was established in 1971 to
monitor the long-term health of workers covered by the
regulations to control occupational exposure to asbestos
[11]. Workers were recruited during, initially, voluntary
and then statutory medical examinations. During the
medical, a brief questionnaire was completed with the
consenting worker and they were then flagged for death
registrations. The results from 1971 to 2005 were published in 2009 [11]. There were 15 496 deaths among the
98 912 workers included in the analysis. All-cause mortality was significantly higher than in the general population. Known associations between asbestos exposure and
mortality from lung, pleural and peritoneal mesothelioma and asbestosis were confirmed. Insulation workers,
stripping/removal workers and those employed in manufacturing asbestos cement had the highest mortality from
asbestos-related disease. In addition, >50% of asbestos
workers were current smokers at the last recorded medical examination, substantially higher than the percentage of smokers in the UK population. Mortality among
smokers was higher than among non-smokers, and some
of the excess deaths among asbestos workers were attributable to smoking.
A recent large-scale report has presented an updated
overview and estimate of the current and future burden
of occupational cancer in Great Britain, based on recent
and current occupational exposures [12]. Lung cancer
and mesothelioma are recognized as important cancer
sites for both men and women in the overall burden,
attributable to specified occupational carcinogens in the
UK. Asbestos contributed the most to both total deaths
attributable to occupational exposure and to cancer registrations (larynx, lung, mesothelioma, stomach). There
are several key exposures which give rise to substantial
exposures across multiple industry sites. Of particular
note is exposure to asbestos in construction, personal
and household services, land transport and mining.
Legislation
The Asbestos Regulations 1969 were passed with the
goal of managing exposure to the dangerous fibres, and
in 1972, there was a voluntary ban on the use of crocidolite. In 1983, the Asbestos (Licensing) Regulations
required a Health and Safety Executive (HSE) licence
for any person working with asbestos coating or asbestos insulation products. This was followed in 1985 by the
UK’s Asbestos (Prohibition) Regulations, which sought
to ban the import or use of the more dangerous forms of
asbestos, namely crocidolite (blue asbestos) and amosite
(brown asbestos). In 1987, the Regulations of 1969 were
replaced by the Control of Asbestos at Work Regulations,
which aimed to ensure tighter controls, focusing on the
prevention of exposure to asbestos while at work [13].
8 Occupational Medicine
The Control of Asbestos at Work Regulations 1987
introduced, in Regulation 16, the statutory requirement
for medical surveillance and the maintenance of health
records. The asbestos employer was required to maintain
a health record for each of their employees exposed to
asbestos above a specified action level. Each employee
exposed to the hazard in this way was required to have
medical surveillance not >2 years before the beginning
of such exposure and periodic medical examinations at
intervals of not >2 years while exposure continued. Each
medical examination included a specific examination of
the chest and employees were issued with a certificate
stating that they had been examined.
The 1987 Regulations were repeatedly amended. In
1992, some usage of white chrysotile asbestos was added
to the prohibition law from 7 years earlier, which had
related to usage and importation of blue and brown
asbestos only [14]. In 1993, the Regulations of 1987 were
amended to necessitate the substitution of any material
containing asbestos.
In the 30 years between 1968 and 1998, it is estimated
that 50 000 people died in the UK from asbestos-related
diseases [15]. Asbestos was responsible for more occupationally induced deaths than any other single cause.
It was recognized that as asbestos could result in death
15–60 years after exposure, the mortality rate would be
expected to rise until at least the year 2010–20 and was
largely determined by the level of exposure before the
introduction in the 1980s of relatively stringent asbestos legislation. It was also recognized that around one
quarter of those dying had once worked in the building
and maintenance trades—where people can be exposed,
often inadvertently, to asbestos during work. The then
Health and Safety Commission (HSC) was concerned
that information on whether buildings have asbestos in
them was not always passed to those at risk.
The Control of Asbestos Regulations 2002 required
a new level of protection for those working in buildingrelated trades and others at risk from asbestos in buildings, by a duty for those with responsibilities for the repair
and maintenance of non-domestic premises to manage
asbestos. It required them to find out if there were asbestos-containing materials within these premises, to record
the location and condition of such materials, and then
assess and manage any risk from them, including passing on information about their location and condition to
anyone liable to disturb them. The regulations applied to
all people with a duty to manage the risks from asbestoscontaining materials in premises: building owners, tenants and anyone else who had any legal responsibilities
for workplaces. The two Approved Codes of Practice
(ACoP) that supported these regulations were revised
also, introducing improved requirements for the provision of training and for clearance procedures following
asbestos work.
Most recently, in 2006, all previous laws on the control of asbestos, including prohibition and licensing regulations, were rolled into the all-encompassing Control
of Asbestos Regulations 2006, which came into force on
13 November 2006 together with the associated Code of
Practice: Work with materials containing asbestos (First
edition 2006) [16]. The earlier codes of practice for work
with asbestos were withdrawn. For the purposes of these
2006 regulations, work with asbestos now included the
removal, repair or disturbance of asbestos, any work
ancillary to and associated with this and supervision of
such work and any associated ancillary work.
The Control of Asbestos Regulations 2012 came
into force on 6 April 2012, updating earlier asbestos
regulations and fully implementing the European Union
Directive on exposure to asbestos (Directive 2009/148/
EC) [3,17]. In practice, the changes are fairly limited
though it does mean that some types of non-licensed
work with asbestos now have additional requirements,
i.e. notification of work, medical surveillance and record
keeping. All other requirements remain unchanged.
Whether a type of asbestos work is licensable, notifiable
but non-licensable, or non-licensed work has to be determined in each case and will depend on the type of work
being carried out, the type of material being worked on
and its condition, and therefore the risk assessment is
key. Full details can be found on the HSE website [18].
Health surveillance and health records
Health records and health surveillance are required by
Regulation 22 of the Control of Asbestos Regulations,
2012 [4,19]. All employees who undertake licensable
work with asbestos (essentially asbestos strippers) and
are exposed to asbestos above a defined action level must
undergo regular health surveillance by a doctor who
has been appointed by the HSE. This must consist of a
2 yearly medical surveillance focussing on the respiratory
system, to include a respiratory questionnaire, respiratory examination and lung function testing (spirometry).
A chest X-ray (CXR) is not a routine part of the examination and should only be done if clinically indicated.
Previous and current exposures must be documented,
including details of any occupational hygiene control
measures when available.
Each employer must keep a health record for any
employee who undertakes licensable work as defined by
the regulations. The health record must be kept in a safe
place for at least 40 years after the last entry put into it
or until the person reaches 80 years. It should contain
certain key pieces of information, including a record of
the types of work carried out with asbestos and where
relevant, its location, with start and end dates, average
duration of exposure in hours/week and details of any
personal protective equipment used.
D. Sen: Asbestos Workers and Their Risks 9
The information that the employee provides to the
appointed doctor as part of the medical surveillance and
any findings or recommendations from the appointed
doctor must be documented in a medical record. The
medical record should be kept by the appointed doctor
as ‘medical in confidence’ in secure storage in line with
professional arrangements.
By 30 April 2015, all workers carrying out Notifiable
Non-licensed Asbestos Work (NNLW) will also need to
have a medical examination. Non-licensed but notifiable
work is essentially any refurbishment activity involving
asbestos—so called ‘white-van-man’ work. Such examinations will then need to be repeated at least every 3 years,
as long as the worker continues to do NNLW. After April
2015, workers carrying out NNLW for the first time will
have to have an examination before they can start such
work. Guidance for doctors conducting these medical
examinations is available on the HSE website [20].
Pathology
Asbestos is dangerous to health for a number of reasons.
The colour of asbestos-containing materials cannot be
used to indicate fibre type and/or toxicity and laboratory
identification is required. Airborne fibres cannot be seen or
smelt. They are characteristically long, thin, respirable particles between 5 and 15 microns long and 0.1 micron thick.
They tend to accumulate in the alveoli adjacent to small
airways, can lodge and penetrate the alveolar wall. Once in
situ, fibres are resistant to destruction, persist in the lung
and provoke low-grade inflammation leading onto fibrosis
[3,7,10]. Fibrosis causes thickening and some narrowing of
the terminal airways. Gradually fibres migrate into the lung
tissue between the alveoli causing an extension of the lowgrade inflammation and interstitial fibrosis develops and
extends to present as asbestosis. Lung cancer and mesothelioma are recognized sequelae to asbestos exposure.
The risk to health is related to both fibre type and
inhaled ‘dose’. It is recognized that larger exposures are
more likely to give rise to more extensive disease but no
low, safe level of exposure has been identified. Expert
medical and epidemiological opinion is that there is no
threshold level of exposure to asbestos below which there
is no risk [1,3,7,21,22]. This is accepted by the courts,
as is the benchmark for a ‘significant’ exposure which
is defined by the Industrial Injuries Advisory Council
(IIAC) as being above normal background levels [23].
As there is a latent period between exposure and illhealth, there are no early health warning signs to alert
the exposed person and in some cases, lung changes can
continue to develop after exposure has ceased.
Asbestos-related health effects
Asbestos exposure can cause four basic types of diseases
as shown in Table 2.
Table 2. Asbestos-related health effects
Benign disease
Pleural plaques
Pleural thickening
Benign pleural effusion
Malignant disease
Mesothelioma
Lung cancer
Interstitial lung disease
Asbestosis
Gastrointestinal disease
Retroperitoneal fibrosis?
Benign pleural disease
Pleural plaques
Pleural plaques are discrete areas of pleural thickening +/–
calcification in the pleura covering the surface of the lung
tissue. They are the most common sequelae of asbestos
exposure and occur in 20–60% of known exposed workers, with a latent period of 10–30 years post-exposure
(prevalence in the general population is 0.5–8%). They
are generally asymptomatic, although rarely cause mild
dyspnoea (shortness of breath) if they are sufficiently
extensive to restrict movement of the underlying lung tissue. Lung function is usually normal and they commonly
occur as calcified areas identified on CXR. They do not
undergo malignant change but their presence indicates
past asbestos exposure [1,2,21,22,24]. The condition
does not constitute a prescribed disease for the purposes
of Industrial Injuries Disablement Benefit (IIDB).
Diffuse pleural thickening
Diffuse pleural thickening occurs usually after more
heavy exposure and pathologically consists of extensive
areas of fibrosis and adhesions [1,2,22,24]. Although
often asymptomatic, it can present with chest pain and
exertional dyspnoea. It can be associated with restrictive
lung function tests and CXR shows extensive shadowing.
It is dose related, the more extensive thickening being
related to more extensive exposure. It is a prescribed
disease.
Benign pleural effusion
Benign pleural effusion(s) are also dose related, usually
after heavier exposure and usually asymptomatic. The
latent period between first asbestos exposure and pleural
effusions is less than for other asbestos-related conditions. It is usually <20 years but can be <10 years postexposure. There is debate over whether benign pleural
effusion can progress to diffuse pleural thickening or
mesothelioma. When a tumour does not develop, it is not
certain whether the finding is coincidental rather than as
a direct progression of the initial pathology [1,2,7,22].
Benign pleural effusion is not a prescribed disease.
10 Occupational Medicine
Benign pleural diseases are not themselves precursors of malignant change but, in so far as they reflect
exposure to asbestos, they may be associated with an
increased risk of asbestos-related pleural malignancy.
The relation between benign pleural disease and lung
cancer is unclear. On a priori grounds, it seems likely
that the risk of malignancy will be more a function of
the dose of asbestos inhaled rather than the presence or
absence of benign pleural disease.
Malignant disease
Malignant mesothelioma
Malignant mesothelioma is an aggressive, diffuse, fatal,
asbestos-associated disease originating from the lining
cells (mesothelium) of the pleural (65–70%), peritoneal
(30%) or, rarely, pericardial (1–2%) cavities around the
lung tissue, abdominal cavity and heart [25]. It has been
recognized as an industrial disease since 1960 when the
strong causative link with asbestos exposure was confirmed [1,8].
Epidemiological data suggest that the amphibole,
crocidolite, is associated with the highest risk of mesothelioma and that the serpentine fibre, chrysotile, has
the lowest. Asbestos exposure is the single major cause
(>90%); however, there is evidence that mesothelioma
may result from both para-occupational exposure, for
example women having laundered their husbands’ overalls, and non-occupational environmental exposure
[1,25,26]. Idiopathic or spontaneous mesothelioma can
also occur in the absence of any exposure to asbestos in
both animals and humans and a recent review suggests a
rate in humans of around one per million [25,27].
Unlike asbestosis, there is no dose–response relationship with mesothelioma: although the risk is very
small at low exposure levels, there is no threshold level
below which there is no risk [1,2,22,25]. There is latency
between initial exposure and disease of 15–60 years,
with a mean of 40 years. One retrospective study found a
median latency of 32 years with 96% of cases occurring
after at least 20 years [1].
It has been typically a disease of dockyard workers,
but other trades are now thought to be at risk including joiners, plumbers, engineers and electricians.
The incidence is increasing. The original UK mesothelioma register dataset, which contained all deaths
from 1968 to 2001, has been superseded by HSE’s
publication Mesothelioma Mortality in Great Britain
1968 to 2012 [28]. It indicates that the annual number
of deaths from mesothelioma rose from 153 in 1968
to 2535 in 2012. From the original data, Hodgson
et al. estimated that deaths from mesothelioma would
peak between the years 2011 and 2015 with between
1950 and 2450 cases annually, but that estimation has
had to be modified to a peak in 2020 of around 2500
deaths [28,29].
In 2009, a case–control study of occupational, domestic and environmental mesothelioma risks in Britain concluded that mesothelioma risk is determined largely by
asbestos exposure before age 30 [30]. The researchers
calculated that men born in the 1940s who worked as
carpenters for >10 years before they reached 30 had a
lifetime risk for mesothelioma of ~1 in 17. For electricians, plumbers and decorators born in the same decade who worked in their trade for >10 years before they
were 30, the risk was 1 in 50 and for other construction
workers, it is ~1 in 10. The report also showed a small,
increased risk in those who had lived with someone who
had been exposed to asbestos.
Early diagnosis is crucial as it is a devastating disease
both physically and psychologically and most patients
will die within a year of diagnosis [1,2,22,27]. Clinically,
it usually presents with a pleural effusion, chest pain
(usually dull, chest wall pain but occasionally sharp,
pleuritic pain) and breathlessness. Radiology will identify the lesions and a histology diagnosis is very helpful
for obtaining appropriate compensation. Currently, the
British Thoracic Society guideline is that a diagnosis
of malignant mesothelioma must be considered in any
patient with a pleural effusion or pleural thickening especially if associated with a history of asbestos exposure
and chest pain [27].
Though there are several recognized treatment options
available, there is little evidence of survival or quality of
life benefits. Active, supportive care is essential to include
interventions for pain relief, dyspnoea and psychosocial
problems. Early diagnosis is essential to reduce suffering,
get early adequate support and compensation. It is a prescribed disease as defined by the IIAC [23].
Lung cancer
Although 90% of lung cancers are associated with smoking, there is evidence of synergy between asbestos and
smoking [1,2,5,8]. Studies suggest that this interaction is
not additive, but with a much greater risk of cancer than
expected taking both risks into account [1,8,31]. There is
no way of distinguishing clinically between primary lung
cancer caused by cigarette smoking from those due to
asbestos or those due to other causes [1,5].
Medical surveillance provides a very important platform for discussion and education of the employee,
to stop smoking and for the employer, to maintain a
smoke free environment. The prognosis of lung cancer
is somewhat worse in a patient with asbestosis as they
may not tolerate surgical or other treatments because of
the underlying disease [1,5,21]. In view of the synergism
between asbestos exposure and smoking, all asbestos
workers, whether they have asbestosis or not, should be
strongly advised to stop smoking.
Darnton et al. [32] have estimated that since the excess
lung cancer risk in heavily exposed workers is likely to be
D. Sen: Asbestos Workers and Their Risks 11
of the same order as deaths from mesothelioma, >1 in 10
of all carpenters born in the 1940s may die of a cancer
caused by asbestos.
Interstitial lung disease—asbestosis
Asbestosis is characterized by chronic pulmonary
interstitial fibrosis and results from exposure to asbestos [1,2,7,21,22]. It develops after a long latency of
25–40 years post-exposure [1,10,21,22]. There is a
dose–response relationship and it is more likely to
occur in those with heavier exposures [33]. It is generally accepted that the development of clinically relevant asbestosis requires a cumulative dose of 25–30
fibres/ml air over many years of exposure [1,3,10,22].
Clinically, it usually presents with gradually developing
dyspnoea and cough and the presence of basal crepitations (crackles heard on auscultation) and finger clubbing (40%). Smoking increases the severity and rate
of deterioration. Up to 40% continue to progress after
removal from exposure and this is more likely to occur
in smokers [34]. The risk of lung cancer is increased
[35,36]. There is no specific treatment or intervention
to halt the disease process and treatment can only be
supportive in the later stages. Regular medical surveillance of exposed workers is very important for early
identification, referral, advice on smoking and removal
from exposure.
Asbestos fibres cause fibrosis of the lungs (asbestosis) and pleura, and cancers as described above, and
have been found in the mesenteric and omental tissue
of patients with mesothelioma and in those exposed to
asbestos through sources other than their occupation.
Therefore, it seems possible that asbestos may be a causal
factor for pleural and retroperitoneal fibrosis [38,39]. In
2004, from a case–control study of 43 patients, Uibu et al.
[39] concluded that occupational asbestos exposure is an
important risk factor for retroperitoneal fibrosis [39].
Screening for asbestos-related disease
Screening is the process of detecting disease before it
becomes symptomatic. For a screening test to be effective, certain criteria must be met regarding the disease,
the proposed test and any treatment that might follow.
Two important principles that must be met are that the
test should have a high accuracy and be available and
affordable; and treatment for the disease(s) must exist
and must be effective before symptoms occur, with little risk or morbidity. Several randomized control trials in
the 1960–80 screened for lung cancer using CXRs and
found no difference in mortality between the screened
and unscreened groups. Also, screening for lung cancer using low-dose computed tomography has not been
proved to be efficacious [40].
Compensation
Gastrointestinal effects
The gastrointestinal tract can be directly exposed to
asbestos when fibres which are deposited in the respiratory tract following inhalation may be swallowed. Some
mortality studies, highlighted in the 1987 IARC review,
have suggested that inhalation of asbestos may cause a
small increase in the incidence of death due to cancer of
the stomach, oesophagus, colon or rectum [7]. However,
a meta-analysis of the available evidence in 1999 concluded that though there was a suggestion of an association between asbestos and laryngeal carcinoma, there
was no evidence that asbestos increased the risk of carcinogenic effects in the gastrointestinal system following
inhalation [37].
Retroperitoneal fibrosis
Retroperitoneal fibrosis is a rare disease characterized
by the presence of retroperitoneal tissue, consisting of
chronic inflammation and marked fibrosis, which often
entraps the abdominal aorta, the ureters and other
abdominal organs with resulting secondary effects. In
~70% of cases, the aetiology is unknown though case
reports and series indicate that it can be induced by
different factors: malignant disease, radiation therapy,
infections and the use of several drugs such as methysergide [38,39].
Patients with asbestos-related lung disease may be
eligible for compensation through IIDB from the
Department of Work and Pensions or a civil law claim
for damages from the employer(s) under whose ‘control’ exposure occurred. Under the Limitation Act 1980,
individuals have 3 years to make a civil claim for personal injuries from the date that they became aware of
any serious injury caused by an act or omission by the
proposed defendant [41]. Benefits may include Personal
Independence Payment which has replaced disability living allowance and Attendance Allowance for those over
65. Various charities can also provide help and support.
Some compensation claims involve protracted investigations (especially civil claims) and patients need to
be warned about this and supported as necessary. It is
important that adequate attention is given to advising
and supporting an affected employee.
Discussion
Asbestos remains the single biggest cause of work-related
deaths in the UK. Significant health risks and serious
diseases result when fibres are inhaled.
There is a large body of available scientific literature,
going back to the 1960s, on cohorts of highly exposed
asbestos workers from which we have convincing
12 Occupational Medicine
evidence of increased mortality from cancers of the lung,
peritoneum and pleura, mesothelioma and asbestosis
that can be caused by this hazard. However, the evidence
is less convincing for cancers in the gastrointestinal tract
as well as other restrictive diseases such as retroperitoneal fibrosis. Currently, asbestos is responsible for ~4500
deaths in the UK every year.
Although it has been many years since the ban on the
use of all forms of asbestos in manufacturing in the UK,
two problems remain: asbestos-related diseases do not
present immediately after exposure and there is often a
latency of many years; and asbestos is present in many
buildings and homes constructed before 2000, which
often results in accidental or inadvertent exposure to
significant levels of airborne fibres when such asbestos
materials are disturbed during construction maintenance and/or refurbishment work. Inadvertent exposure
to asbestos is a cause of great concern to those affected.
The asbestos removal worker is particularly vulnerable
but other workers in any trade are at risk when asbestos
is disturbed and must be protected. Although the type
of asbestos involved and duration of exposure may be
known, there is often little reliable information about
the level of exposure. These are all important factors in
determining the level of risk, but immediate medical surveillance is not the answer. HSE provides guidance on its
website on what to do in such situations [42].
An efficacious screening test that could result in early
detection of asbestos-related diseases such as lung cancer, malignant mesothelioma and asbestosis and reduced
mortality would represent a major advance in combating
mortality (and morbidity). Unfortunately, even for lung
cancer, the most common cancer worldwide, screening
cannot be recommended [40].
There has been much debate about the usefulness of
the statutory health surveillance of asbestos workers as
required under current UK health and safety legislation.
Although screening of workers during their working life
alone is unlikely to detect some of the more serious longlatency diseases such as lung cancer and malignant mesothelioma, screening has some benefits [43]. It provides
opportunities for workplace interventions to prevent further exposure, referral for non-medical (compensation
and disability) services for those with asbestos-related
disease, identifies additional groups at risk of asbestosrelated disease and introduces modifications of current
exposure conditions, life style factors and smoking cessation when appropriate. Components of the medical
assessment should include the histories (especially smoking and lifetime occupational history), physical examination and diagnostic evaluation [43].
Are there any gaps in the evidence base? Two specific
areas where there has been insufficient research done,
and more would therefore be useful, are, firstly, in relation to finding a reliable health surveillance tool (with
high specificity and sensitivity) for the early detection of
asbestos-related lung diseases in particular and secondly,
to determine whether there is a level of asbestos fibresin-air that might actually be safe for human health.
Key points
•• Asbestos,
sometimes described as ‘the hidden
killer’, remains the single biggest cause of workrelated deaths in the UK and possibly worldwide.
•• Currently in the UK, asbestos-related deaths each
year number 4500 and the peak in the number
dying of diseases associated with asbestos exposure is expected to be reached between the years
2015 and 2010.
•• Asbestos-related diseases often have a long latency
of many years duration, thus making hazard association difficult.
•• Disease progression often continues well after
exposure has ceased, usually to a serious (asbestosis) if not fatal (mesothelioma and lung cancer)
conclusion.
•• Treatment options in serious asbestos-related diseases (asbestosis, malignant mesothelioma) are
limited.
•• With a ban on asbestos usage in the UK, accidental, inadvertent asbestos exposure remains the
biggest problem now, particularly in the maintenance, repair and refurbishment of old buildings
harbouring asbestos. Second-hand exposure from
handling contaminated work clothes should also
not be ignored.
Conflicts of interest
None declared.
References
1. Baxter PJ, Aw TC, Cockcroft A, Durrington P, Harrington
JM, eds. Hunter’s Diseases of Occupations. 10th edn. London:
Hodder Arnold Press, 2010; 990–1010.
2.Currie GP, Watt SJ, Maskell NA. An overview of how
asbestos exposure affects the lung. BMJ 2009;339:b3209.
3. Leman RA, Dodson RF. Asbestos. In: Bingham E, Cohrssen
B, eds. Patty’s Toxicology. 6th edn. New York: J Wiley & Sons
Inc., USA, 2012; 211–256.
4.HSE. The Control of Asbestos Regulations 2012. Statutory
Instruments. http://www.legislation.gov.uk/uksi/2012/632/
contents/made (24 June 2014, date last accessed).
5.Nielsen LS, Bælum J, Rasmussen J et al. Occupational
asbestos exposure and lung cancer—a systematic review of
the literature. Arch Environ Occup Health 2014;69:191–206.
6.Wagner JC, Newhouse ML, Corrin B, Rossiter CE,
Griffiths DM. Correlation between fibre content of the
lung and disease in east London asbestos factory workers.
Br J Ind Med 1988;45:305–308.
D. Sen: Asbestos Workers and Their Risks 13
7.IARC. IARC Monograph Volume 100C: Asbestos (Chrysotile,
Amosite, Crocidolite, Tremolite, Actinolite and Anthophyllite).
http://monographs.iarc.fr/ENG/Monographs/vol100C/
mono100C-11.pdf (12 May 2014, date last accessed).
8. McDonald C. Asbestos. In: McDonald C, ed. Epidemiology
of Work Related Diseases. 2nd edn. London, UK: BMJ
Publishing Group, 2000; 85–108.
9. Wagner JC, Sleggs CA, Marchand P. Diffuse pleural mesothelioma and asbestos exposure in the North Western Cape
Province. Br J Ind Med 1960;17:260–271.
10.Doll R, Peto J. Asbestos: Effects on Health of Exposure to
Asbestos. London: HMSO, 1985.
11. Harding AH, Frost G. The Asbestos Survey. Mortality Among
Asbestos Workers 1971–2005. Prepared by the Health and
Safety Laboratory for the Health and Safety Executive,
HSE Books 2009 [Research Report RR730]. http://www.
hse.gov.uk/research/rrpdf/rr730.pdf (28 June 2014, date
last accessed).
12.Rushton L, Bagga S, Bevan R et al. The Burden of
Occupational Cancer in Great Britain. Overview Report.
Prepared by the Health and Safety Laboratory, the Institute
of Environment and Health, the Institute of Occupational
Medicine and Imperial College London for the Health
and Safety Executive, HSE Books 2012 [Research Report
RR800]. http://www.hse.gov.uk/research/rrpdf/rr800.pdf
(25 June 14, date last accessed).
13. The Control of Asbestos at Work Regulations 1987. Statutory
Instrument 1987 No. 2115. http://www.legislation.gov.uk/
uksi/1987/2115/made (11 May 2014, date last accessed).
14.
The Control of Asbestos at Work (Amendment)
Regulations 1992. Statutory Instrument 1992 No. 3068.
http://www.legislation.gov.uk/uksi/1992/3068/contents/
made (11 May 2014, date last accessed).
15. HSE press release E239:02 - 16 December 02. http://www.
hse.gov.uk/press/2002/e02239.htm.
16. HSC. Work With Materials Containing Asbestos. Control of
Asbestos Regulations, 2006. Approved Code of Practice and
Guidance. London, UK: HSE Books, 2006. http://www.aber.
ac.uk/en/media/departmental/healthsafetyenvironment/asbestos_l143_2006_gen.pdf (2 June 2014, date last accessed).
17. Directive 2009/148/EC of the European Parliament and of the
Council of 30 November 2009 on the Protection of Workers
From the Risk Related to Exposure to Asbestos at Work. http://
eur-lex.europa.eu/LexUriServ/LexUriServ.do?uri=OJ:L:2009
:330:0028:0036:EN:PDF (2 June 2014, date last accessed).
18. HSE website. http://www.hse.gov.uk/asbestos/licensing/
notifiable-non-licensed-work.htm (2 June 2014, date last
accessed)
19. HSE. Guidance for Appointed Doctors on the Control of
Asbestos Regulations 2012. Medical Surveillance for Workers
Carrying Out Licensed Work With Asbestos. MS31 (rev. 1).
June 2012. http://www.hse.gov.uk/pubns/ms31.pdf (18
May 2014, date last accessed).
20. HSE. Guidance for Doctors on the Control of Asbestos
Regulations 2012. Medical Surveillance for Workers Carrying
Out Non-Licensed Work With Asbestos. MS34. June 2012.
http://www.hse.gov.uk/pubns/ms34.htm (18 May 2014,
date last accessed).
21. Health Protection Agency. Asbestos: Toxicological Overview.
Prepared by Bull S, HPA 2007, version 1. http://www.hpa.
org.uk/webc/HPAwebFile/HPAweb_C/1202487029823
(25 June 2014, date last accessed).
22.Smedley J, Dick F, Sadhra S. Chapter 2 – Chemical hazards. In: Oxford Handbook of Occupational Health. Oxford:
Oxford University Press, 2013.
23.Department of Work and Pensions. IIAC Report 2005.
London, UK: The Stationery Office [TSO], 2005. http://
iiac.independent.gov.uk/pdf/command_papers/Cm6553.
pdf (18 May 2014, date last accessed).
24.Fishwick D, Barber CM. Non-malignant asbestos-related
diseases: a clinical view. Clin Med 2014;14:68–71.
25. Moore AJ, Parker RJ, Wiggins J. Malignant mesothelioma.
Orphanet J Rare Dis 2008;3:34.
26. Howel D, Gibbs A, Arblaster L et al. Mineral fibre analysis and
routes of exposure to asbestos in the development of mesothelioma in an English region. Occup Environ Med 1999;56:51–58.
27.Wiggins J. BTS statement on malignant mesothelioma in
the UK, 2007. Thorax 2007;62(Suppl. 2):ii1–ii19.
28. HSE. Mesothelioma in Great Britain 2014. Mesothelioma
Mortality in Great Britain 1968 to 2012. http://www.hse.gov.
uk/statistics/causdis/mesothelioma/mesothelioma.pdf
(2
June 2014, date last accessed).
29.Hodgson JT, McElvenny DM, Darnton AJ, Price MJ,
Peto J. The expected burden of mesothelioma mortality in Great Britain from 2002 to 2050. Br J Cancer
2005;92:587–593.
30. Peto J, Rake C, Gilham C, Hatch J. Occupational, Domestic
and Environmental Mesothelioma Risks in Britain, a CaseControl Study. Prepared by the Institute of Cancer Research
and the London School of Hygiene and Tropical Medicine
for the Health and Safety Executive, HSE Books 2009
[Research Report RR696]. http://www.hse.gov.uk/research/
rrpdf/rr696.pdf (11 June 2014, date last accessed).
31. Lee PN. Relation between exposure to asbestos and smoking jointly and the risk of lung cancer. Occup Environ Med
2001;58:145–153.
32.Darnton AJ, McElvenny DM, Hodgson JT. Estimating
the number of asbestos-related lung cancer deaths
in Great Britain from 1980 to 2000. Ann Occup Hyg
2006;50:29–38.
33. Berry G, Gilson JC, Holmes S, Lewinsohn HC, Roach SA.
Asbestosis: a study of dose-response relationships in an
asbestos textile factory. Br J Ind Med 1979;36:98–112.
34.Bégin R, Sébastien P. Excessive accumulation of asbestos
fibre in the bronchoalveolar space may be a marker of individual susceptibility to developing asbestosis: experimental
evidence. Br J Ind Med 1989;46:853–855.
35. Banks DE, Mei-Lin W, Parker JE. Editorial. Asbestos exposure, asbestosis and lung cancer. Chest 1999;115:320–322.
36.Hillerdal G, Henderson DW. Asbestos, asbestosis, pleural plaques and lung cancer. Scand J Work Environ Health
1997;23:93–103.
37.Goodman M, Morgan RW, Ray R, Malloy CD, Zhao K.
Cancer in asbestos-exposed occupational cohorts: a metaanalysis. Cancer Causes Control 1999;10:453–465.
38. Sauni R, Oksa P, Järvenpää R, Parker JE, Roto P. Asbestos
exposure: a potential cause of retroperitoneal fibrosis. Am
J Ind Med 1998;33:418–421.
39.Uibu T, Oksa P, Auvinen A et al. Asbestos expo
sure as a risk factor for retroperitoneal fibrosis. Lancet
2004;363:1422–1426.
40.Silvestri GA, Alberg AJ, Ravenel J. The changing epidemiology of lung cancer with a focus on screening. BMJ
2009;339:b3053.
14 Occupational Medicine
41. Legislation.gov.uk. Limitation Act 1980. http://www.legislation.gov.uk/ukpga/1980/58/part/I/crossheading/actions-inrespect-of-wrongs-causing-personal-injuries-or-death (13
July 2014, date last accessed).
42. HSE website. http://www.hse.gov.uk/asbestos/faq.htm (2
June 2014, date last accessed)
43.Levin SM, Kann PE, Lax MB. Medical examination for
asbestos-related disease. Am J Ind Med 2000;37:6–22.
doi:10.1093/occmed/kqu195
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