MINI-SYMPOSIUM: PATHOLOGY OF NON-NEOPLASTIC LUNG DISEASE
The pathology of asbestosis
Richard L Attanoos
Allen R Gibbs
Abstract
The term asbestosis refers to diffuse interstitial pulmonary fibrosis conse-
quent to the excess inhalation of asbestos fibres. It is a disease associ-
ated with heavy cumulative asbestos dose and the latent period, from
initial exposure to disease manifestation, is long usually 20 years or
more, with an inverse correlation with dose. Because heavy industrial ex-
posures have diminished the incidence of asbestosis has decreased.
Asbestosis is a divisible disease with the frequency and severity of dis-
ease correlating with cumulative asbestos dose. Disease severity also cor-
relates with asbestos fibre type (amphiboles more potent than
commercial chrysotile), immune and genetic factors. Pathologically,
there are two components to the diagnostic criteria which must be met:
first, the presence of diffuse interstitial lung fibrosis of an appropriate
pattern; and second, some tissue marker of excess asbestos inhalation
either requisite numbers of asbestos bodies (as determined by light mi-
croscopy) or elevated asbestos fibres (as determined by mineral anal-
ysis). The clinical picture is not specific although in contrast to
idiopathic pulmonary fibrosis, which is the most frequent diagnostic prob-
lem, asbestosis has a slowly progressive course over decades. Lung can-
cer occurs at cumulative asbestos doses similar to that necessary to
cause lung fibrosis (asbestosis). The main differential diagnoses with
asbestosis are idiopathic pulmonary fibrosis, pulmonary fibrosis associ-
ated with connective tissue disorders, chronic phase hypersensitivity
pneumonitis and silicate (mica, talc, kaolin) pneumoconiosis.
Keywords asbestos; asbestosis; interstitial lung disease; pathology
Introduction
Asbestos is a general term applied to certain fibrous forms of
various silicate minerals which have crystallized in nature pro-
ducing fibres of high tensile strength and flexibility, a feature
which is important in its commercial applications.1 Asbestos
occurs in one of two forms: serpentine and amphibole. Chrysotile
is the only serpentine form of asbestos and comprises 90% of all
asbestos used in most countries. The major amphiboles that have
been used commercially are amosite, crocidolite, anddto a much
lesser degreedanthophyllite. Non-commercial amphiboles
include tremolite and actinolite. The physicochemical differences
between amphiboles and chrysotile are distinct and underpin
their significant different biological toxicities. Amphibole fibres
Richard L Attanoos BSc MB BS FRCPath is a Consultant Histopathologist at
University Hospital, Llandough, Cardiff, UK. Conflicts of interest: none
declared.
Allen R Gibbs MB BCH FRCPath is a Consultant Histopathologist at University
Hospital, Llandough, Cardiff, UK. Conflicts of interest: none declared.
DIAGNOSTIC HISTOPATHOLOGY 19:8
are straight and rigid with long biopersistence in tissues (years to
decades) whereas chrysotile fibres are curled, pliable with short
biopersistence in tissues (weeks to months) (Figures 1e3). The
persistence of respirable bio-active fibres is the single most
important factor in the development of asbestos-related diseases
whether neoplastic or non-neoplastic. Because of its physico-
chemical properties, chrysotile asbestos is most suitable for
making fabrics, other flexible items and also used in friction
product manufacture. The amphiboles with superior chemical
and physical stability were used often with chrysotile to make
various asbestos-cement products, insulation pipes and boards,
roofing and fire-proofing materials.
Historically, asbestosis was the first asbestos-related disease
recognized. Dr. Montague Murray, has been generally credited as
the first person to report the disease in 1899, with the term
asbestosis coined in 1925 by Oliver and again used in 1927 by
Cooke.2 The links between asbestos and lung cancer in the
presence of asbestosis were suggested and disputed a decade
later and firmly established in 1955 by Doll.3,4 For mesothelioma
the association with asbestos was suggested in 1960 by Wagner
and co-workers in his case series of persons in the crocidolite
mining district of Griqualand West in the North West Province of
South Africa.5
The adverse risks of asbestosis have been effectively
controlled by the workplace changes introduced by the 1931
Asbestos regulations and again by the more stringent 1969
Asbestos regulations. These allowed the continued use of
asbestos only if maximum allowable concentrations of dust were
not exceeded and if other precautions were maintained. In the
1970s, 1980s, and 1990s further restrictions, both voluntary and
statutory, were placed on the importation and use of asbestos.
This has resulted in a dramatic decrease in the number of
symptomatic cases of asbestosis in the developed countries. In
July 1999, the European Commission announced a European
Union ban on all remaining chrysotile use by 1 January 2005. In
the United States, Occupational Safety and Health Administration
(OHSA) introduced a range of controls for asbestos. The current
OSHA airborne permissible exposure limit (PEL) (introduced in
1994) is set at 0.1 fibre/ml (for all fibre types). Life-long exposure
to asbestos at these permissible levels is considered sufficient to
prevent the manifestation of asbestosis.
It has long been known that amphibole asbestos dust expo-
sure constitutes a significant danger to health. However, some
critical issues still remain in scientific dispute, including the
relative hazards of different types of asbestos and whether there
is a safe level of exposure to any of them. Nowadays, the major
adverse health effects of asbestos are related to increased risk of
cancer especially malignant pleural mesothelioma following low
dose exposures from brief, intermittent sources to amphibole
asbestos in populations of persons previously not considered ‘at
risk’ of developing fatal asbestos-related diseases.
Clinico-radiological features
The clinical presentation of asbestosis is typically insidious with
shortness of breath on exertion and a dry cough. Auscultation
may reveal late inspiratory crackles initially in the postero-lateral
regions of the lower zones but later becoming more widespread
as the disease progresses. In advanced stages cyanosis and
cardiorespiratory failure may occur.
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 MINI-SYMPOSIUM: PATHOLOGY OF NON-NEOPLASTIC LUNG DISEASE

Figure 1 Chrysotile asbestos fibres (TEM). Figure 3 Crocidolite asbestos fibres (TEM).

Lung function tests show a restrictive pattern with impair- causation of the lung fibrosis because the pleura is far more
ment of gas transfer but there may be an element of airflow sensitive to the injurious effects of asbestos than the lung pa-
limitation. renchyma. Accordingly, the same lack of significance may be
Generally asbestosis is characterized by lower lobe involve- stated for exposed persons with lung cancer and pleural changes.
ment and small irregular opacities. Progression will result in The light microscopic findings of asbestosis are now well
thickening of the linear opacities and the development of hon- established and defined by the recent 2010 College of Patholo-
eycombing particularly in the sub-pleural region of the lower gists e Pulmonary Pathology Society (CAP-PPS) Asbestosis
lobes. Pleural abnormalities such as diffuse pleural fibrosis or Guidelines committee.6 First there is a requirement to confirm
plaques may be present. the presence of diffuse interstitial fibrosis of an appropriate
pattern described as ‘always acellular and collagenous rather
Pathology than fibroblastic and inflammatory’. The second component is
the presence of a necessary minimum number of either asbestos
Asbestosis is characterized by diffuse interstitial fibrosis of the
bodies or fibres (see below). The aforementioned asbestosis
lungs, particularly with involvement of the lower zones and with
sub-pleural accentuation (Figures 4). In advanced cased the
lungs have a firm consistency with a bosselated surface and have
a greyewhite cut surface with areas of honeycombing. Purulent
secretions may be seen indicating complicating pneumonia. Firm
mass lesions may suggest complicating neoplasia. There may or
may not be associated pleural thickening and/or plaques. The
presence of pleural changes is a neutral factor in determining the

Figure 4 Lung showing fibrosis and honeycombing (asbestosis) most

Figure 2 Amosite asbestos fibres (TEM). marked in the lower zones and sub-pleurally.

DIAGNOSTIC HISTOPATHOLOGY 19:8 283 Ó 2013 Published by Elsevier Ltd.

 MINI-SYMPOSIUM: PATHOLOGY OF NON-NEOPLASTIC LUNG DISEASE
pattern translates, in effect to a fibrotic phase non-specific
interstitial pneumonia-like (N.S.I.P.-like) morphology and this
consideration is useful as it contrasts with other common dif-
ferentials e.g. Usual Interstitial Pneumonia (U.I.P) and hyper-
sensitivity pneumonitis, both of which are fibroblastic and
inflammatory in nature, notwithstanding other significant dif-
ferences.7,8 The presence of fibroblastic ‘buds’ and cellular
interstitial infiltrates are so uncommon in asbestosis as to suggest
an alternate diagnosis, namely U.I.P. There is medical debate
whether the pattern of fibrosis alone is sufficiently robust a
feature to indicate an alternate diagnosis to asbestosis, irre-
spective of asbestos biomarkers (asbestos body counts and fi-
bres) or whether U.I.P. asbestosis exists in certain persons
exposed to asbestos. It would seem logical that U.I.P. could
sometimes occur in heavily exposed asbestos workers unrelated
to asbestos exposure since they have a similar risk to the general
population of developing U.I.P.
The assessment of ‘diffuse interstitial fibrosis’ is not simple
and prompts the requirement to examine multiple tissue blocks,
in general at least 10 samples should be examined (central and
peripheral from each lobe) although there is a recognition that
this may not be possible in resection specimens. Small biopsies
(transbronchial and even open lung wedge specimens) are very
limited in predicting pneumoconiosis and unsuitable for mineral
analyses (see later). The presence of cancer, atelectasis and
bronchopneumonia may all hinder the assessment of back-
ground interstitial fibrosis. Extensive areas of organizing diffuse
alveolar damage in post mortem lungs cause problems in
assessing how much chronic interstitial fibrosis is present e this
can often be resolved by correlation with sequential radiological
findings if available. Collagen stains may assist but are often
inconclusive in problematic cases.
In the early stages of asbestosis, the fibrosis appears airway-
centric only with early alveolar duct fibrosis (grade 1 fibrosis).
Bronchiolar wall fibrosis alone is now not regarded as bonafide
asbestosis, a new development departing from the previous 1982
College of Pathologists e National Institute Occupational Safety
and Health (CAP-NIOSH) Asbestosis committee report.9 As with
many pneumoconioses the disease distribution is actually lym-
phangiocentric in nature, around broncho-vascular bundles,
septa and pleura and this explains the accentuation of disease in
these regions. Asbestosis is a true dose dependent disease. With
increasing cumulative asbestos dose so the interstitial fibrosis
(grade) advances and this is accompanied by increased numbers
of asbestos bodies and amphibole fibres in lung. Grade 3 fibrosis
shows true ‘bridging fibrosis’ and grade 4 fibrosis represents
honeycomb lung (Table 1). It is at these pathological levels of
fibrosis (grades 3 and 4) that clinical manifestations of disease
exist. It has been estimated that persons with clinical asbestosis
have prior cumulative exposures of at least 25 fibre/ml years.
This cumulative dose is regarded as the same necessary to double
the relative risk of lung cancer in exposed persons (even in the
absence of asbestosis). Grade 1 and 2 fibrosis is sub-clinical
(pathological) asbestosis which may manifest at lower cumula-
tive exposures. However grade 1 and 2 fibrosis is more difficult to
assess, being subtle and common in the lungs of urban dwellers
and in tobacco smokers. Considerable caution should be exer-
cised by the pathologist in making a diagnosis of early/mild
asbestosis in an asbestos exposed person with a history of
DIAGNOSTIC HISTOPATHOLOGY 19:8
Asbestosis (fibrosis) grades
Grade 1 Fibrosis involving the bronchiolar wall and
first layer of alveoli
Grade 2 Fibrosis involving bronchioles and more
distant alveolar walls but not linking up with
each other
Grade 3 Fibrosis involving all alveoli between two
adjacent bronchioles but with little
architectural distortion
Grade 4 Widespread fibrosis usually with
honeycombing
Table 1
tobacco smoking in the presence of focal interstitial fibrosis
associated with numerous intra-alveolar pigment laden macro-
phages and respiratory bronchiolitis (RBILD). This smoking
related interstitial lung disease is a common pitfall because the
fibrosis is not fibroblastic and not inflammatory (in the inter-
stitium). Smoking is also likely to induce more advanced fibrosis,
possibly honeycombing, in a proportion of cases. A U.I.P.
morphology has been described, distinct from that described in
the vast majority of asbestosis cases. Langerhans cell histiocy-
tosis may produce chronic stellate fibrotic lesions with pauci-
cellular infiltrates of Langerhans cells (CD1aþ, S100þ,
Langerinþ). We have seen occasional cases of Langerhans His-
tiocytosis mis-diagnosed as asbestosis, particularly when there is
extensive fibrosis and the focal collections of Langerhans cells
and eosinophils have been largely lost. Close attention to the
pattern of fibrosis will make it unlikely to be confused with that
seen in asbestosis but may mimic that of mixed dust fibrosis
(mixed silica and less fibrogenic mineral agents e see later)
(Figures 5e8).
The second essential component to allow for a diagnosis of
asbestosis is the presence of necessary numbers of either
asbestos bodies (assessed by light microscopy) or fibres
(assessed by mineral analysis). With respect to asbestos body
counts, their assessment may be enhanced by Perls stained
Figure 5 Moderate interstitial fibrosis and numerous asbestos bodies.
284 Ó 2013 Published by Elsevier Ltd.
 MINI-SYMPOSIUM: PATHOLOGY OF NON-NEOPLASTIC LUNG DISEASE
Figure 6 Same as Figure 5 but at higher power.
routine thickness (5 micron) sections. The average (arithmetic
mean) number is calculated by counting all present within the
available lung section area. For bonafide asbestosis, an average
rate of >2 asbestos bodies/cm2 section area is necessary (in the
presence of diffuse interstitial fibrosis). Most persons with
bonafide asbestosis meet these morphological criteria set by the
2010 CAP-PPS Asbestosis committee. In most persons there is a
correlation between inhaled and retained amphibole asbestos
fibres and asbestos body counts. However, very rare cases, so-
called occult asbestosis, do arise in which persons with significant
asbestos exposure have diffuse interstitial fibrosis but with
inadequate numbers or no asbestos bodies. Due to an immune
lysosomal dysfunction the host has an innate inability to form
asbestos bodies. The mineralogical demonstration of an elevated
amphibole asbestos fibre count is necessary to prove significant
asbestos exposure in these rare individuals.
Care must be taken when interpreting ferruginous body counts
because the Perls stain will identify a wide range of iron staining
material and small fragments (without asbestiform morphology)
should not be counted. Strict adherence should be attained to
counting only those dumbbell, beaded bodies formed on
Figure 7 Classical asbestos bodies with straight clear fibrous cores.
DIAGNOSTIC HISTOPATHOLOGY 19:8
transparent cores. A range of non-asbestos minerals may form
similar ferruginous bodies; some may mimic asbestos bodies with
transparent cores (erionite) whereas others are platy-form with
brown cores (silicates such asmica, talc, kaolin), some have black
cores (coal, metals) and some are wavy (elastin). In some com-
plex exposures (e.g. welders, foundry workers), mixed ferrugi-
nous bodies may occur and this necessitates mineral analysis to
allow for an accurate diagnosis because it is not possible to count
the true asbestos bodies accurately using light microscopic means.
In general, interstitial fibrosis is not marked in persons
following silicate exposures but so-called silicatoses e kaoli-
nosis, talcosis and mica pneumoconiosis e have been reported
in association with very heavy exposures.10 The presence of
interstitial fibrosis and ferruginous bodies (albeit qualitatively
different from true asbestos bodies) may represent a pitfall to the
unwary pathologist. Silicatoses may show varying degrees of
lung and pleural fibrosis. Exposures to other minerals such as
quartz and feldspar may also occur and histologically be asso-
ciated with prominent refractile particulates and granulomatous
reactions. Talc is a mineral widely used in the ceramic, paper,
plastics, rubber, paint, and cosmetic industries. The distinct
forms of pulmonary disease caused by talc have been defined
according to route of administration.11 Talcosis may follow pure
industrial exposure or seen in association with asbestos and sil-
ica exposures. The particle size is finer than that observed with
‘mainline’ talc granulomatosis following intravenous drug abuse,
although the condition has been reported as a radiological mimic
of asbestosis. Ferruginous bodies have been detected in persons
following talc pleurodesis for the management of chronic effu-
sions, a consideration of importance in persons with mesotheli-
oma as there may be false ascription to asbestos.
Mineralizing pulmonary elastosis (endogenous pneumoconi-
osis) seen in persons with chronic haemorrhagic disorders,
chronic cardiac failure and obesity/chronic sleep apnoea may
develop lung fibrosis, encrustation of elastic fibres with the for-
mation of pseudoasbestos bodies, and may be a pitfall in the
diagnosis of asbestosis.12,13 Mineral analysis is useful in con-
firming the fibre content.
Mineral analysis plays a central role in the diagnosis of
asbestosis. Numerous studies have shown a correlation between
Figure 8 Mica ferruginous bodies from a case of mica induced pneumo-
coniosis showing platy cores.
285 Ó 2013 Published by Elsevier Ltd.
 MINI-SYMPOSIUM: PATHOLOGY OF NON-NEOPLASTIC LUNG DISEASE
grade of lung fibrosis and retained amphibole asbestos fibre count.
There is no correlation with chrysotile asbestos fibre counts
because the fibres are not biopersistent. Fibre deposition does vary
across the lung so ‘pooled’ samples comprising three 2e3 cm3
samples of lung or 2e3 standard lung paraffin lung blocks are
optimal for the analytical process. By this process the intra-
laboratory variation is no more than 2e3 fold. All laboratories
must establish control reference ranges for non-occupational
exposed persons and for subjects with asbestosis. The latter con-
stitutes the laboratory ‘asbestosis range’, a value now regarded of
important diagnostic and medico-legal interest with regard to the
causation of lung cancer in the absence of asbestosis. The range
has to be established for each laboratory because preparation,
instrumentation and counting protocols vary between laboratories.
The asbestosis range represents the total retained amphibole
asbestos fibre count collated amongst all persons (all grades)
with morphological degrees of asbestosis (according to the 2010
CAP-PPS criteria e listed above). Chrysotile fibre counts are
excluded. As qualitative fibre typing is necessary and such in-
formation is only available in electron microscopic mineral
analytical methods, the asbestosis range cannot be effectively
established by using phase contrast light microscopy. The latter
method is too blunt a tool to identify the majority of asbestos
fibres in the respirable bio-active fraction.
Differential diagnoses
The clinical factors in asbestosis offer little to allow for a specific
diagnosis. Typically there is a slow tempo of disease over de-
cades. The exposure history is important but this may be difficult
to quantify even in experienced hands. Clinical assessments
require history taking and recollection of exposures many de-
cades prior to the onset of disease. However, because of the
relatively high exposures to asbestos required to produce clinical
asbestosis it is unlikely that an individual would struggle to recall
a substantial exposure to asbestos. Indeed if there is such a
problem of recall one should be very circumspect in diagnosing
asbestosis. With bonafide asbestosis now a disappearing disease
in the developed western countries, the most common dilemma
which now emerges is elderly persons who fall out with classical
‘at risk’ occupations for asbestosis who have atypical clinical
presentations and pathology. In many cases the clinical history is
rapid (over 3e5 years) like idiopathic pulmonary fibrosis and the
pathology is that of typical U.I.P. Variable numbers of asbestos
bodies and fibres are detected but are rarely significantly elevated
underpinning the inconstant relationship between cumulative
dose, grade of fibrosis, asbestos body count and amphibole
asbestos fibre burden expected in typical asbestosis. When there
is a history of asbestos such cases have been termed ‘atypical
asbestosis’ by some, or conversely, idiopathic pulmonary fibrosis
(U.I.P. pathology) in an asbestos exposed subject. U.I.P. is a
temporally (mature fibrosis and immature fibroblastic ‘buds’)
and spatially (normal lung juxtaposed to honeycomb lung) het-
erogeneous process contrasting with asbestosis (and N.S.I.P.)
temporally and spatially homogeneous in nature.
Some persons with chronic hypersensitivity pneumonitis
develop a U.I.P. or N.S.I.P. morphology and asbestosis may be
suspected in exposed persons. In hypersensitivity pneumonitis,
the lymphocytic infiltrate is typically florid in nature and other
features such as giant cells with cholesterol clefts, minute
DIAGNOSTIC HISTOPATHOLOGY 19:8
airway-centric granulomas and areas of organizing pneumonia
may suggest the diagnosis. Allergen testing is important.
Pleuro-pulmonary manifestations of collagen vascular disease
may mimic asbestos-related disease, not only by inducing lung
fibrosis (directly or via treatments such as methotrexate) (either
indistinguishable N.S.I.P. less often U.I.P.) but also by inducing
diffuse pleural fibrosis. Serological tests are important in estab-
lishing these diagnoses. Pathologists are minded to look for spe-
cific features which may indicate a connective tissue disease. For
rheumatoid arthritis: rheumatoid necrobiotic nodules, vasculitis,
follicular bronchiectasis/bronchioloectasis. For ankylosing spon-
dylitis, the disease has an upper zone predilection. For Sjo €gren’s
syndrome, the disease typically manifests as lymphocytic inter-
stitial pneumonia. The history of connective tissue disease makes
the confirmation of asbestosis problematic in an exposed person.
There is the basic requirement to consider the pattern of fibrosis
and doseeresponse profile observed in asbestosis in association
with the known biomarkers (asbestos bodies and fibres). Funda-
mentally, is the degree of fibrosis commensurate with the expo-
sure, asbestos body and fibre counts? If so, the condition is likely
asbestosis. If there is an atypical fibrotic process or fibrosis is in
excess of that expected then it is likely that a significant contri-
bution from a non-asbestos factor is present.
Some fibrosing lung conditions have an upper zone predilection,
for example sarcoidosis, Langerhans cell histiocytosis and anky-
losing spondylitis; this is in contradistinction to asbestosis. Focal
interstitial fibrosis and scars as seen in apical fibroelastosis, tuber-
culosis, healed organized pneumonia, healed infarct, rounded
atelectasis, pulmonary hyalinized granuloma should similarly be
discounted and are wholly inconsistent with asbestosis. In a person
with a history of prior irradiation, radiation pneumonitis/fibrosis
may show central zone predilection of disease. A
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DIAGNOSTIC HISTOPATHOLOGY 19:8
Practice points
C The development of asbestosis is associated with latent pe-
riods often in excess of 20 years.
C The rate of clinical progression of asbestosis is typically very
slow occurring over several years.
C Asbestosis typically shows the most severe changes in the
lower zones of the lungs and sub-pleurally.
C Histological diagnosis of asbestosis requires the presence of
an appropriate pattern of diffuse interstitial fibrosis and a
sufficient number of asbestos bodies (>2/cm2).
C The presence of fibroblastic foci and/or cellular interstitial in-
filtrates militates against a diagnosis of asbestosis.
287 Ó 2013 Published by Elsevier Ltd.