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Reviews and Commentary 

State of the Art: Imaging of
Occupational Lung Disease1

n  State of the Art

Christian W. Cox, MD
Imaging of occupational lung disease, often perceived as
Cecile S. Rose, MD, MPH
a static discipline, continues to evolve with changes in in-
David A. Lynch, MB
dustry and imaging technology. The challenge of accurately
identifying an occupational exposure as the cause of lung
disease demands a team approach, requiring integration
of imaging features with exposure type, time course, and
severity. Increasing use of computed tomography has dem-
onstrated that specific occupational exposures can result
in a variety of patterns of lung injury. The radiologist must
understand the spectrum of expected imaging patterns
related to known occupational exposures and must also
Online CME recognize newly described occupational exposure risks,
See www.rsna.org/education/search/ry
often related to recent changes in industrial practices.

Learning Objectives: © RSNA, 2014

After reading the article and taking the test, the reader will
be able to:
n Categorize the broad spectrum of imaging patterns
from lung injury caused by occupational exposures
to provide a novel framework for approaching
occupational lung disorders.
n Discuss guidelines permitting the use of digital
radiography in the International Labor Organization
classification of pneumoconioses.
n Explain the importance of a multidiscipline approach to
occupational lung disease.
n Identify newly recognized occupational lung diseases
such as accelerated silicosis in denim sandblasting
and deployment-related lung disease to highlight the
dynamic nature of the field.
Accreditation and Designation Statement
The RSNA is accredited by the Accreditation Council for
Continuing Medical Education (ACCME) to provide continuing
medical education for physicians. The RSNA designates this
journal-based CME activity for a maximum of 1.0 AMA PRA
Category 1 Credit TM. Physicans should claim only the credit
commensurate with the extent of their participation in the
activity.
Disclosure Statement
The ACCME requires that the RSNA, as an accredited
provider of CME, obtain signed disclosure statements from
the authors, editors, and reviewers for this activity. For this
journal-based CME activity, author disclosures are listed at
the end of this article.

1
 From National Jewish Health, 1400 Jackson St, Denver,
CO 80206-2761. Received July 19, 2012; revision
requested September 4; revision received December 20;
final version accepted January 30, 2013; final review
November 11. Address correspondence to C.W.C.
(e-mail: coxc@njhealth.org).

q
 RSNA, 2014

Radiology: Volume 270: Number 3—March 2014  n  radiology.rsna.org 681

STATE OF THE ART: Imaging of Occupational Lung Disease Cox et al
W
ith advances in technology over
the past 40 years, radiology has
increasingly become pivotal in
management of most common medical
conditions, including stroke, chest pain,
cancer, and trauma. In contrast, the role
of radiology in the diagnosis and treat-
ment of occupational lung disease ap-
pears at first glance to have changed very
little. Despite substantial limitations, ra-
diography remains the most widely used
method for diagnosis and monitoring of
many occupational lung diseases, often in
conjunction with the International Labor
Organization (ILO) classification system
(1). In many settings, radiologists prac-
tice at a distance from their occupational
medicine or pulmonary colleagues (2),
Essentials
nn The emphasis on the spectrum of
lung injury caused by occupational
exposures provides a novel frame-
work for approaching occupa-
tional lung disorders.
nn New guidelines permitting the
use of digital radiography in In-
ternational Labor Organization
classification of pneumoconioses
are discussed and additional
online resources are provided.
nn Reviewing new occupational lung
diseases such as accelerated sili-
cosis in denim sandblasting and
deployment-related lung disease
reveals the dynamic nature of the
field.
nn Restructuring imaging character-
istics in occupational lung disease
into a pattern-based approach
stresses the variability in imaging
appearances and provides a foun-
dation for the radiologist to pro-
spectively consider an occupa-
tional exposure as a cause of an
undiagnosed lung disease.
nn Expanding knowledge of thin-
section CT characteristics of oc-
cupational lung disease furthers
understanding of the pathophysi-
ology of these diseases and em-
phasizes the limitations of the
current radiograph-based
classification of pneumoconioses.
682 radiology.rsna.org  n  Radiology: Volume 270: Number 3—March 2014
relying on typical imaging appearances
and the clinical history, rather than inter-
disciplinary interaction, to suggest the
diagnosis of occupational lung disease.
Since the approach to classifying occupa-
tional lung disease is often based mainly
on exposure history rather than imaging
pattern (3–6), the radiologist may be at a
further disadvantage in recognizing an
imaging abnormality as work related.
In fact, the diagnosis and imaging of
occupational lung diseases is rapidly
evolving. Thin-section computed tomog-
raphy (CT) of the chest continues to
demonstrate previously unidentified
characteristics that shape our under-
standing of occupational lung injury (7–
11). New industrial practices and mate-
rials are increasingly recognized as causes
of lung disease (12–18). Less-industrial-
ized nations may enforce fewer protective
regulations, so that “exporting” more
hazardous industrial processes may re-
sult in outbreaks of occupational lung dis-
eases that are now rare in the United
States (6,17,18). Moreover, recurrent or
distinct radiographic appearances in the
setting of a common exposure have aided
in the identification of several newer oc-
cupational exposures which cause lung
disease (12–16).
In this article, we demonstrate the
importance of a multidisciplinary ap-
proach to diagnosis of occupational lung
disease, with particular emphasis on a
radiologic pattern-based approach. We
illustrate the spectrum of lung injury re-
lated to occupational exposures and dis-
cuss the imaging features of several newly
described occupational diseases.
Clinical Evaluation
The Occupational and Environmental
Exposure History
To recognize a lung disease as work re-
lated, the clinical findings must be in-
formed by specifics of workplace expo-
sures along with the relevant medical and
scientific literature on causal associations
between exposures and associated health
effects. A detailed medical and exposure
history remains the mainstay of diagnosis
of exposure-related lung disease. The
medical history should include the onset
and timing of the patient’s chest symp-
toms, past medical history, review of
systems, current medications, family his-
tory, and personal habits, including use of
tobacco products, alcohol, and recrea-
tional drugs. The three essential compo-
nents of an occupational history include
(a) a chronology of current and longest
held jobs, (b) a current job description,
and (c) questions about symptoms during
or after exposure to specific fumes, dusts,
and chemicals. For example, in patients
presenting with symptoms of interstitial
lung fibrosis, the clinician should elicit in-
formation about previous exposure to fi-
brogenic dusts such as asbestos, silica,
and coal mine dust. Other clinical clues
that may suggest an exposure-disease
link include a temporal relationship be-
tween an exposure and respiratory symp-
toms (eg, work-related wheezing in an
auto-body worker exposed to isocya-
nates), a diagnosis that has been strongly
linked to exposure (eg, pleural mesotheli-
oma), or the unexpected occurrence of
an illness (eg, lung cancer in a non-
smoker). Such findings should prompt
the physician to obtain a more thorough
occupational history, with a detailed de-
scription of all jobs held, associated expo-
sures, and presence of similar illness
among coworkers. Table 1 contains some
of the more common exposures associ-
ated with risk for occupational lung dis-
eases, along with typical imaging findings.
Information on nonoccupational ex-
posures, particularly those in the home
environment and associated with particu-
lar hobbies or recreational activities, also
should be elicited. The presence of ani-
mals can be important in understanding
risk for hypersensitivity pneumonitis
(from birds or feather furnishings) or
asthma (eg, from pet dogs and cats). Use
of indoor hot tubs and exposure to other
Published online
10.1148/radiol.13121415  Content codes:
Radiology 2014; 270:681–696
Abbreviations:
ILO = International Labor Organization
NSIP = nonspecific interstitial pneumonia
PMF = progressive massive fibrosis
UIP = usual interstitial pneumonia
Conflicts of interest are listed at the end of this article.
STATE OF THE ART: Imaging of Occupational Lung Disease Cox et al

potentially contaminated aerosol sourc-
es (eg, those from humidifiers or mois-
ture intrusion in the home) should be
sought when hypersensitivity pneumoni-
tis is a diagnostic consideration, as ex-
posure abatement is necessary for
disease management. Finally, the ciga-
rette smoking history must be elicited
since clinical and imaging findings may
be partially or entirely explained by to-
bacco smoke exposure.
Physical Examination
Findings at lung examination are gener-
ally nonspecific and often occur late in
the course of chronic occupational pul-
monary diseases. For interstitial diseases,
inspiratory crackles on auscultation re-
flect later stages of fibrosis and may be
accompanied by digital clubbing and find-
ings of right heart failure. For occupa-
tional airways diseases, physical examina-
tion findings are often normal. Wheezing
may be a sign of large airways obstruc-
tion, and end-inspiratory squeaks may be
heard in patients with bronchiolitis.
Laboratory Testing
Depending on the disease of concern, se-
rologic and other laboratory studies may
help distinguish exposure-related lung
diseases from autoimmune and other
conditions that may be included in the

Table 1
Imaging Features That May Be Identified Following Specific Common Exposures
Exposure Airway Parenchyma Pleura Risk for Lung Malignancy

Coal mine dust
Respirable silica
Fibrogenic asbestos
Organic and inorganic
 antigens
Beryllium
Flavoring chemicals
 (diacetyl); oxides of
nitrogen and sulfur;
combustion products
Chemical irritants and
  toxic fumes
Bronchial wall thickening
Bronchial wall thickening
Bronchial wall thickening
Bronchial wall thickening
Airway wall thickening
Mosaic attenuation,
  air trapping
Airway wall thickening,
 bronchiectasis, mosaic
attenuation, air trapping
Upper lobe small nodular Conglomerate opacities may
  opacities (simple coal worker’s   mimic solitary mass
 pneumoconiosis)
Lower lobe irregular opacities
Coalescent large opacities (PMF)
Emphysema
Silicoproteinosis Pleural thickening Risk for lung cancer
Upper lobe small nodular Pleural effusions Conglomerate opacities may
  opacities (simple silicosis)   mimic solitary mass
Lower lobe irregular opacities
Coalescent large opacities (PMF)
Emphysema
Asbestosis: Lower lobe or Pleural effusion Risk for lung cancer
  diffuse irregular opacities Pleural plaques (calcified Pleural mesothelioma
Rounded atelectasis   and noncalcified)
Diffuse pleural thickening
  (involving the
  costophrenic angle)
Mesothelioma (irregular
  nodularity of pleura)
Nonfibrotic hypersensitivity
  pneumonitis: centrilobular
  nodules; ground glass
  opacities; thin-walled cysts;
 emphysema
Emphysema
Fibrotic hypersensitivity
 pneumonitis: volume loss;
diffuse reticular opacities;
modest mediastinal
adenopathy; honeycombing
Perilymphatic nodules Risk for lung cancer
Conglomerate opacities
Centrilobular nodules
High dose: chemical pneumonitis

Radiology: Volume 270: Number 3—March 2014  n  radiology.rsna.org 683

STATE OF THE ART: Imaging of Occupational Lung Disease Cox et al
differential diagnosis. For example, a pos-
itive blood beryllium lymphocyte prolifer-
ation test is helpful in distinguishing
chronic beryllium disease from sarcoido-
sis (19,20).
Pulmonary Function Testing
Pulmonary function tests are essential to
determining lung disease pathophysiol-
ogy, severity, management, response to
treatment, prognosis, and impairment.
Full pulmonary function tests include
measurements of lung volume, pre- and
postbronchodilator spirometry, and diffu-
sion capacity for carbon monoxide. Occu-
pational lung diseases are often charac-
terized as obstructive, restrictive, or a
combination of both. Cardiopulmonary
exercise testing can be helpful in deter-
mining the presence and degree of venti-
latory and gas exchange abnormalities, in
clarifying the presence of cardiac disease
as a source of chest symptoms, and in
determining lung disease severity and im-
pairment. Methacholine challenge is use-
ful in establishing the presence of airways
hyperreactivity in some occupational air-
ways diseases (21). Interpretation of pul-
monary function test results may be fur-
ther enhanced when considered in
relation to CT data. For example, sub-
jects with normal spirometry findings but
low lung diffusion capacity may have
mixed emphysema and lung fibrosis evi-
dent on CT scans.
Bronchoscopy and Surgical Lung Biopsy
A careful exposure history in combina-
tion with imaging and pulmonary func-
tion testing is often enough to make the
diagnosis of an occupational lung disease.
This is particularly true for the pneumo-
conioses, which usually manifest with dis-
tinct imaging abnormalities and typical
occupational histories. Similarly, occupa-
tional asthma and most other obstructive
lung diseases are diagnosed without his-
tologic findings. When diagnostic uncer-
tainty remains, clinicians may need to
consider lung biopsy. Fiberoptic bron-
choscopy, with bronchoaveolar lavage
and transbronchial biopsies, is particu-
larly useful in the evaluation of exposure-
related granulomatous lung dis­ease such
as chronic beryllium disease and hyper-
sensitivity pneumonitis. Surgical lung bi-
684 radiology.rsna.org  n  Radiology: Volume 270: Number 3—March 2014
opsy may be required to confirm a diag-
nosis of bronchiolitis or in cases in which
diagnostic certainty is important for man-
agement in the clinical setting of diffuse
interstitial lung disease.
Imaging Technology
The chest radiograph remains the pri-
mary mode of screening for pneumoconi-
osis in the United States and elsewhere.
Its advantages are relatively low cost, low
radiation dose, and wide availability.
However, the chest radiograph is rela-
tively insensitive for detecting early pneu-
moconiosis (21–24). The chest radio-
graph is particularly insensitive for
abnormalities such as ground-glass opac-
ity found in granulomatous occupational
diseases like hypersensitivity pneumoni-
tis and chronic beryllium disease (25,26).
An abnormal chest radiograph is also
relatively nonspecific for diagnosis of
pneumoconiosis, since a substantial pro-
portion of cases identified as demonstrat-
ing pneumoconiosis on chest radiographs
are found to have no evidence of pneu-
moconiosis at CT (27–30) or autopsy
(31). This lack of specificity may in part
be due to the fact that cigarette smoking
causes small irregular opacities on chest
radiographs (32). Additionally, the
boundary between normal and abnormal
chest radiographs may be subjective and
difficult to define (33).
A systematic classification system for
chest radiographic findings in pneumoco-
nioses was first developed more than 50
years ago and has been repeatedly re-
vised by the ILO with support from the
National Institute for Occupational Safety
and Health (NIOSH) and the American
College of Radiology (1,34,35). By pass-
ing a NIOSH-administered film-based ex-
amination, physicians may become certi-
fied “B-readers,” permitting them to
apply the systematic ILO clas­si­fication to
interpret screening chest radiographs for
pneumoconiosis. The sys­tem uses a set of
22 standard radiographic images to cod-
ify and characterize the presence, pat-
tern, and extent of pleural and parenchy-
mal abnormalities related to occupational
exposures. An important recent develop-
ment is the adaptation of the analog-
based system to a digital format, with the
recent release of a digital set of standard
images (27) and publication of proposed
guidelines permitting the use of digital ra-
diography systems for evaluation of coal
miners (36). Free customized viewing
software to facilitate side-by-side viewing
of digital chest images and digital stan-
dards may be downloaded at the Centers
for Disease Control and Prevention Web
site (37).
Thin-section CT has replaced chest
radiography in evaluation of nonoccupa-
tional diffuse lung diseases because of its
higher sensitivity for early lung disease
and greater accuracy in characterizing
the pattern of disease (38,39). Despite
these advantages, no country has adopt-
ed CT as a primary screening modality
for pneumoconiosis, presumably because
of higher cost and radiation dose com-
pared with chest radiography. CT is com-
monly used as a secondary screening mo-
dality in symptomatic or physiologically
impaired workers when the chest radio-
graph is normal or equivocal (40). CT is
particularly useful in identifying and char-
acterizing atypical presentations of occu-
pational lung dis­ease, as discussed below.
A standardized system for scoring extent
of disease on CT scans, analogous to the
ILO radiographic classification system, is
increasingly used (40–44) and has been
shown to be associated with moderate
interreader and intrareader agreement
for all categories of abnormality except
ground-glass abnormality (45). Reduced-
dose CT (,1.5 mSv) is beginning to be
used to screen for lung cancer in those
with occupational exposures creating
high risk for malignancy (particularly as-
bestos exposure) (46,47). In such individ-
uals, CT may also be used to screen for
pneumoconiosis.
The Radiologist’s Role
As with many lung diseases, diagnosis of
occupational lung disease requires a mul-
tidisciplinary approach, including the oc-
cupational medicine physician, radiolo-
gist, industrial hygienist, pulmonologist,
and pathologist. Traditionally, the radiol-
ogist assists in confirming a suspected
diagnosis correlated with the clinical his-
tory with or without lung biopsy—an ap-
proach which has left the radiologist no-
STATE OF THE ART: Imaging of Occupational Lung Disease Cox et al

ticeably absent from the initial recognition Table 2

of new occupational lung diseases, de-
spite the routine use of imaging in the Pattern-based Approach to Differential Diagnosis of Occupational Lung Disease
diagnosis (12–15). Looking to the future, Pattern Classic Presentation Atypical Presentation
the radiologist is well positioned to iden-
tify clusters of radiographic patterns that Diffuse pulmonary opacity
 Consolidation Acute silicosis (3,4,6,57); Hard metal lung (3,4,6,134);
may lead to identification of new occupa-
Hypersensitivity pneumonitis (5,6,57); Flock worker’s lung (15,16)
tional exposures or new sources of known
Ardystil syndrome (5,56)
exposures. For example, multidetector
  Ground glass Hypersensitivity pneumonitis (4–6,60–64,77); Chronic beryllium disease
CT played a central role in the identifica-
Acute silicosis (3,4,6,57); (3–5,9,67,68);
tion and characterization of accelerated Hard metal (3,4,6,66,134); Asbestosis (3,4,6,8,69);
silicosis in Turkish denim sandblasters Flock worker’s lung (15,16); Siderosis (3,5,6,134);
(48,49). Diffuse pleural thickening, iden- Indium-tin oxide (12,132) Accelerated silicosis (49)
tified on chest radiographs in workers   Crazy paving Acute silicosis (3,4,57);
and residents in Libby, Montana, was an Indium-tin oxide (12)
important marker of exposure to vermic- Nodules
ulite contaminated with amphibole as-  Centrilobular Acute silicosis (3,4,57); Chronic silicosis
bestos (50–54). Hypersensitivity pneumonitis (4–6,60– (3,4,6,11,49);
CT evaluation may assist in differenti- 64,73,77); Coal worker’s
ating between occupational lung disease Siderosis (3,5,6,74,134); pneumoconiosis (3,4,6,10);
and other common causes of respiratory Flock worker’s lung (15,16); Aluminosis (134);
impairment, such as smoking-related Ardystil syndrome (5,56); Hard metal lung (66)
lung disease. At the same time, radiolo- Indium-tin oxide (12);
gists must realize the broad spectrum of Byssinosis (6);
appearances of occupational lung disease Accelerated silicosis (49)
at imaging. Occupational injury can be  Perilymphatic/subpleural Chronic silicosis (3,4,6,11,22,69,82); Hard metal lung (4,65);
Coal worker’s pneumoconiosis (3,4,6,10,28); Aluminosis (134);
generally categorized into airspace, nodu-
Chronic beryllium disease (3–5,9,67); Accelerated silicosis
lar, reticular, cystic, emphysematous, air-
Talcosis (71,135); (48,49);
way, and pleural patterns which correlate
Calcicosis (5); Asbestosis (4,8,75)
with particular exposures. Table 2 pro-
Stannosis (72)
vides an extensive, though not exhaus- Fibrosis
tive, list of exposures categorized by im-  UIP/NSIP Asbestosis (3,4,6,8,75); Chronic silicosis (4,11);
aging pattern on CT scans or chest Hypersensitivity pneumonitis (4–6,60–64) Coal worker’s
radiographs. pneumoconiosis (4,28);
Chronic beryllium disease
Diffuse Pulmonary Opacities (3–5,9,67);
Diffuse pulmonary opacities, including Hard metal lung
consolidation, ground-glass opacities, (3,4,6,66,136);
and crazy paving, may represent a wide Siderosis (3,6,134);
gamut of histologic patterns, including Ardystil syndrome (5);
diffuse alveolar damage (13), organizing Flock worker’s lung (15,16);
pneu­monia (5,55,56), and alveolar pro- Indium-tin oxide (24);
teinosis (3,4,12,57,58). As a classic ex- Aluminosis (134)
ample, acute silicosis or silicoproteinosis Masses
manifests as multifocal consolidations  PMF/conglomerate Complicated silicosis (3,4,6,11,22,69); Siderosis (3,134);
with posterior distribution (Fig 1), occa- Complicated coal worker’s pneumoconiosis Chronic beryllium disease
(3,4,6,28); (3–5,67)
sionally with a nodular component
Talcosis (3,5,71,135)
(3,4,57,58). Diffuse pulmonary opac-
  Round atelectasis Asbestos exposure (4,6,75) Silicosis (11)
ities in the setting of an occupational
exposure do not necessarily imply acute Table 2 (continues)
lung disease. Development of consolida-
tive opacities from organizing
pneumonia in a series of Spanish textile Several occupational exposures (4,5,60–64) and hard metal intersti-
workers in 1992 was attributed to Acra- characteristically cause ground-glass tial lung disease (65,66). Other expo-
min-FWN exposure and later termed opacities on CT scans, such as hyper- sures like accelerated silicosis (49),
Ardystil syndrome (5,55,56,59). sensitivity pneumonitis (Fig 2) asbestosis (8), and chronic beryllium

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STATE OF THE ART: Imaging of Occupational Lung Disease Cox et al

Table 2 (continued) Figure 1 

Pattern-based Approach to Differential Diagnosis of Occupational Lung Disease

Pattern Classic Presentation Atypical Presentation

  Bronchogenic carcinoma Asbestos exposure (3,4,6,75) Silicosis (3,4);

Airway abnormalities
  Mosaic attenuation/air Hypersensitivity pneumonitis (4,5,60–62);
trapping Flavor worker’s lung (4);
Toxic fume inhalation (6,83);
Occupational asthma (137)
 Bronchiectasis Toxic fume inhalation (6,83)
  Bronchial wall thickening Occupational asthma (138,139);
Toxic fume inhalation (6);
Chronic beryllium disease (3–5,9,67)
Emphysema Coal worker’s pneumoconiosis (3,4,10,28,76);
Talcosis (injected) (3);
Siderosis (3,5,134)
Cysts Hypersensitivity pneumonitis (4,5,60,77)
Pleural abnormalities
  Pleural plaques/thickening Asbestos exposure (4,6,75);
Chronic silicosis (4,11,49,69);
Accelerated silicosis (49)
 Pseudoplaques Chronic silicosis (3,4);
Chronic beryllium disease (5,9,67);
Coal worker’s pneumoconiosis (4,28)
  Pleural effusion Asbestos exposure (4,6,75);
Acute silicosis (57)
 Mesothelioma Asbestos exposure (4,6,75)
Lymph nodes
 Lymphadenopathy Chronic silicosis (3,4,22);
Chronic beryllium disease (3–5,9,67,68);
Hypersensitivity pneumonitis (4);
Accelerated silicosis (49)
  Hyperdense or calcified Chronic silicosis (3,4,6,22);
lymph nodes Acute silicosis (57);
Chronic beryllium disease (5,9);
Coal worker’s pneumoconiosis (6,28)
Coal worker’s
pneumoconiosis (3,4);
Hard metal lung (3)
Asbestosis (4,6,8);
Silicosis (82)
Figure 1:  Thin-section CT image at the level of
Silicosis (82) the right middle lobar bronchus in a patient with
concentrated concrete dust exposure resulting in
Flavor worker’s lung (4)
acute silicosis that manifested as posterior predomi-
nant patchy consolidation. Note some areas of
ground-glass opacity and septal thickening consis-
Hypersensitivity pneumonitis
tent with a crazy-paving pattern (between arrows).
(4,62);
Silicosis (4,22,49,69,76,82);
Asbestosis (8);
Chronic beryllium disease (9); Figure 2 
Hard metal lung (65,134);
Talcosis (inhaled) (71,135)
Calcicosis (5);
Siderosis (134)
Chronic silicosis (11) Figure 2:  Thin-section CT image through the lung
bases in a patient with hypersensitivity pneumonitis
demonstrates bibasilar ground-glass opacities and
some focal mosaic attenuation (arrow).
Coal worker’s pneumonitis
(3,28);
Acute silicosis (57) Figure 3 
Accelerated silicosis (49);
Aluminosis (140)

Note.—Numbers in parentheses represent reference numbers.

disease (9,67,68) occasionally demon- The crazy-paving pattern, described

strate ground-glass opaci­ties, usually
in combination with more character-
istic findings. Processes that may
mimic airspace patterns include con-
glomerate fibrosis (Fig 3), rounded
atelectasis, and malignancy.
as well-defined regions of ground-glass
opacity with superimposed septal thick-
ening, scattered throughout regions of
normal-appearing lung, has been asso-
ciated with silicoproteinosis in some
but not all studies (57).
Figure 3:  Thin-section CT image at the level of
the carina in a foundry worker with complicated
silicosis demonstrates conglomerate opacity in the
posterior right upper lobe (arrow) with volume loss
consistent with progressive massive fibrosis (PMF).

686 radiology.rsna.org  n  Radiology: Volume 270: Number 3—March 2014

STATE OF THE ART: Imaging of Occupational Lung Disease Cox et al

Figure 4  Figure 5 

Figure 5:  Thin-section CT image just superior to the

carina in a patient with occupational beryllium expo-
sure demonstrates perilymphatic distribution of fine
nodularity with nodules studding the fissures (black
arrow) and the bronchovascular bundle (white arrow).

beading, bronchovascular studding, and

subpleural nodularity. Silicosis and coal
worker’s pneumoconiosis most often
produce well-defined perilymphatic
nodules or combined centrilobular and
subpleural nodules (3,4,22,28,49,69,70),
as do most other pneumoconioses
Figure 4:  Thin-section CT images at the level of the left lower lobar bronchus in a patient (3,5,71,72). Early pneumoconiosis
with a 20-year history of metal mining. (a) Uniform distribution of well-defined centrilobular tends to be more centrilobular (Fig 4)
nodules is present. (b) Seven years later, the pattern transitions to perilymphatic nodules with (30). Centrilobular nodularity in sub-
peripheral (black arrow) and bronchovascular (white arrow) distribution. There is a new conglomerate jects with subacute hypersensitivity
mass in the superior segment of left lower lobe. pneumonitis, acute silicosis, hard metal
disease, and siderosis tends to be less
Figure 6  well defined or ground glass in appear-
ance (3–5,57,58,60–66,73,74). Perilym-
phatic distribution of nodules similar to
sarcoidosis is seen with chronic beryl-
lium disease (Fig 5) (3–5,9,67,68).
Characteristic differences in the
distribution of nodularity reflect impor-
tant differences in pathophysiology be-
tween the various occupational lung dis-
eases, but it is important to remember
that substantial overlap may occur.

Reticular Patterns
Reticular linear opacities may represent
Figure 6:  Thin-section CT images in a patient with occupational asbestos exposure.
fibrosis occurring in asbestosis (Fig 6a),
(a) Basilar peripheral predominant reticular pattern (black arrows) and traction bronchi-
chronic hypersensitivity pneumonitis,
ectasis (white arrow) are present consistent with asbestosis. (b) Image through the left
and in some patients with respirable sil-
upper lobe in bone window reveals associated calcified pleural plaque (arrowhead).
ica or coal mine dust exposure. Typical
appearances of usual interstitial
Nodular Patterns sides within the central secondary pul- pneumonia (UIP) and nonspecific inter-
When evaluating nodular lung disease, monary lobule, sparing the subpleural stitial pneu­monia (NSIP) may be seen,
distinction between centrilobular versus region. Conversely, perilymphatic nod- but the find­ings in early pneumoconio-
perilymphatic or random distribution is ules are distributed along the axial and sis may be less specific. Certain radio-
important. Centrilobular nodularity re- peripheral interstitium, with septal logic characteristics may help differen-

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STATE OF THE ART: Imaging of Occupational Lung Disease Cox et al
Figure 7  Figure 8  bronchiolitis in military personnel re-
Figure 7:  Thin-section CT image through the right
upper lobe in a coal miner shows confluent centri-
lobular emphysema (between arrows).
tiate potential exposures. For example,
although asbestosis typically manifests
as a UIP pattern, subpleural dotlike or
branching opacities and parenchymal
bands are more common than in idio-
pathic pulmonary fibrosis (8,75). Addi-
tionally, because pleural plaques occur
at a much lower fiber burden than as-
bestosis, interstitial fibrosis from asbes-
tos exposure is uncommon in the ab-
sence of pleural plaques (Fig 6b). The
presence of lobular decreased attenua-
tion, air trapping, or predominance of
disease in the upper or midlungs should
suggest fibrotic hypersensitivity pneu-
monitis (4,5,60,61,63).
Emphysema and Cysts
Several studies describe emphysema as-
sociated with occupational lung disease,
particularly silicosis or coal worker’s
pneu­ moconiosis (4,22,69,76). Centri-
lobular and panacinar emphysema are
present in higher rates in coal workers
(Fig 7) or silica exposed individuals
than in the general population, even
when adjusting for smoking history
(69), and may be found in nonsmokers.
Paracicatricial emphysema, defined as
emphysema resulting from fibrosis and
architectural distortion, may also occur
in relationship to PMF. Peripheral cystic
688 radiology.rsna.org  n  Radiology: Volume 270: Number 3—March 2014
Figure 8:  Thin-section CT image at the level of
the bronchus intermedius in a patient with hyper-
sensitivity pneumonitis demonstrates scattered cysts
(arrows). Note the characteristic centrilobular
ground-glass nodules near the horizontal fissure
(between arrowheads).
spaces, which may represent paraseptal
emphysema or fibrotic-related changes,
have been reported in hard metal inter-
stitial lung disease (65,66), and scat-
tered cysts have been described in
subacute hypersensitivity pneumonitis
(Fig 8) (4,5,77). Interestingly, emphy-
sema has also been described as one of
the more common manifestations of
chronic hypersensitivity pneumonitis on
long term follow-up, even in non-
smokers (62,78–80).
Airway Patterns
Small airway disease typically manifests
as centrilobular nodules, centrilobular
ground-glass opacities, or mosaic perfu-
sion with air trapping. Mosaic perfu-
sion (sharply defined heterogeneity of
lung attenuation) and air trapping sug-
gest hypersensitivity pneumonitis or
constrictive bronchiolitis (Fig 9). “Fla-
vor worker’s lung” or “popcorn work-
er’s lung” associated with artificial but-
ter flavoring results in constrictive
bronchiolitis manifesting as mosaic per-
fusion and air trapping (4). Recently,
concerns have arisen regarding risk of
turning from deployment in Iraq and
Afghanistan (81). Abnormalities of
small airway disease have also been de-
scribed in other occupational lung dis-
eases, such as asbestosis and silicosis
(4,8,82).
Large airway disease manifested by
means of imaging findings of peribron-
chial thickening and bronchiectasis may
be associated with inhalation of toxic
fumes (Fig 10) and with other causes of
occupational asthma (83). Large airway
changes may be also found in chronic
beryllium disease (3,4,9), silicosis or
coal worker’s pneumoconiosis (49,76)
and constrictive bronchiolitis (14), al-
though not as the dominant pattern.
Pleural Patterns
Benign pleural abnormalities (including
effusion, diffuse pleural thickening, or
pleural plaques) are most commonly as-
sociated with asbestos exposure
(3,5,75,84,85). Pleural effusions typically
arise within 10–15 years and pleural
thickening or plaques generally arise 20–
30 years after initial exposure (Fig 11)
(8). In silicosis, parenchymal pseudo-
plaques secondary to coalescence of
subpleural nodules may be seen (3–5),
and more recently silicosis has also
been shown to be associated with true
pleural abnormality, including pleural
thickening, effusion, and pleural invagi-
nation (11).
Major Contemporary Occupational
Lung Diseases
Silicosis
Although the incidence of silicosis has
fallen since its peak during World
War II, it is still a major cause of pul-
monary impairment in at-risk
workers. Occurrence of new cases of
silicosis may be due to inadequacy of
current respirable dust limits or fail-
ure to control workplace exposure to
respirable silica. In addition to the
classic occupational settings for silico-
sis risk in miners, foundry workers,
and sandblasters, silicosis may also
occur in ceramic (86) or construction
STATE OF THE ART: Imaging of Occupational Lung Disease Cox et al

Figure 9 

Figure 9:  Thin-section CT images at the level of the bronchus intermedius in a flavor industry worker with bronchiolitis oblit-
erans. (a) Inspiratory image with subtle mosaic attenuation. (b) Expiratory image shows air trapping in adjacent areas of the
right upper, middle, and lower lobes (between arrows), and also in the left lung.

Figure 10  Figure 11  sion tomography (PET) scans (Fig 12)
Figure 10:  Thin-section CT image through the
right middle and lower lobes in a patient with re-
mote work-related high-dose anhydrous ammonia
exposure resulting in bronchiectasis (arrowhead),
bronchial wall thickening (black arrow), and mosaic
attenuation (white arrow), indicating a combination
of large and small airways abnormality.
workers (87). A newly recognized
cause of accelerated silicosis and sili-
coproteinosis is sandblasting denim
clothing, mainly in developing coun-
tries where few exposure controls ex-
ist (17,18,48,88). In a study of former
denim sandblasters, chest radio-
graphic evidence of silicosis was found
Figure 11:  Axial CT image at the basilar seg-
mental bronchi in soft-tissue window demonstrates
predominantly calcified bilateral pleural plaques
(arrowheads), consistent with asbestos-related pleu-
ral disease.
in 77 of 145 subjects (18). Other
newly recognized occupational groups
at risk for silicosis include goldwork-
ing jewelers (89) and electric cable
manufacturers (90).
Centrilobular and perilymphatic
nodules are characteristic of silicosis.
Nodal enlargement with or without
nodal calcification may also be seen
(91). Emphysema (22,92) and expira-
tory gas trapping (82) are important
contributors to physiologic impairment.
Conglomerate masses occur typically in
the posterior upper lobes or superior
segments of lower lobes (93) and are
often hypermetabolic on positron emis-
(3,94,95). Slowly progressive fibrosing
interstitial pneumonia with a pattern
typical of UIP may occur in about 10%
of silicosis patients (Fig 13) (96,97).
The prevalence of pleural abnormality
in silicosis has been underemphasized;
silicosis is associated with unexplained
pleural effusions in 11% and pleural
thickening in 58% of subjects (11).
Rounded atelectasis may also be seen
(98,99). In acute or subacute silicopro-
teinosis, consolidation is characteristic.
Crazy-paving pattern may or may not
be seen, and other findings may include
centrilobular nodules and pulmonary
calcifications (57).
Coal Worker’s Pneumoconiosis
Despite knowledge of risk factors and
implementation of dust control
measures, increasing prevalence of
pneumoconiosis among underground
U.S. coal miners has been identified
in several recent publications. Wade
et al (100) reported 138 newly identi-
fied cases of coal workers pneumoco-
niosis—related PMF in West Virginian
coal miners from 2000 to 2009, with
21 deaths. Nearly all miners in this
group who developed PMF experi-
enced exposures following implemen-
tation of federal dust regulations.
Laney et al (101) also report increased
prevalence of pneu­ moconiosis in un-
derground coal miners from 1980 to
2008. Additionally, regional increases

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STATE OF THE ART: Imaging of Occupational Lung Disease Cox et al

Figure 12  Figure 13 

Figure 13:  Thin-section CT image through the

lung bases in a coal worker shows peripheral basilar
predominant reticulation (arrows) with subtle honey-
combing (arrowhead) consistent with a UIP pattern
of interstitial fibrosis.

Figure 12:  Hard rock miner with complicated silicosis. (a) Thin-section CT image through the right upper peated inhalation of and sensitization to
lobe shows conglomerate opacity (arrow) with surrounding nodularity. Note the presence of both cicatricial a wide variety of organic aerosols and
and centrilobular emphysema. (b) Fused PET/CT image at the same level demonstrates increased metabolic some chemical antigens. Diagnosis relies
activity in the conglomerate opacity, with a maximum standardized uptake value of 8.8. on a constellation of features including
antigen exposure, characteristic signs
and symptoms, pulmonary function ab-
in prevalence of coal workers pneu- countries, CT-based studies have shown normalities, radiologic abnormalities,
moconiosis in Appalachia have been substantial prevalence of asbestos-relat- and histologic findings (116). Work-relat-
reported (102). ed disease in current and former asbes- ed exposures important in development
The imaging features of coal work- tos workers (108,109). A recent CT of hypersensitivity pneumonitis include
er’s pneumoconiosis are similar to study of 1011 asbestos-exposed workers microbially-contaminated metal-working
those described for silicosis. A substan- showed that 47% had pleural plaques fluids, isocyanates used in two-part
tial minority (10%–40%) of coal miners and 6% had asbestosis (109). There is paints, and organic dusts in farming,
affected by coal worker’s pneumoconio- increased concern about environmen- among many others. However, no clear
sis develop diffuse lung fibrosis, charac- tally acquired asbestos-related disease. causal antigen can be identified in a sub-
terized on the chest radiograph by For example, in Libby, Montana, a signif- stantial minority of cases. In a series of
small irregular opacities in the lower icant increase in mortality from lung 85 consecutive cases of hypersensitivity
lungs (99,103,104). These irregular cancer, mesothelioma, and asbestosis pneu­ monitis presenting to the Mayo
opacities correlate better than rounded occurred in miners and community resi- Clinic, avian antigens accounted for 29
opacities with the extent of physiologic dents owing to locally mined vermiculite cases (34%), with hot tub lung in 18
impairment (105). On chest CT scans, contaminated with small amounts of (21%) and farmer’s lung in nine (11%)
this entity is characterized by reticular tremolite asbestos (Fig 14) (110–112). In (117). No cause was identified in 21
abnormality often associated with hon- this population, the presence of radio- cases (25%). Regardless of the antigen,
eycombing, similar to UIP or NSIP graphic pleural disease was associated typically only a minority of exposed indi-
(106,107). Reticular abnormality may with restrictive lung function (113). In viduals will develop hypersensitivity
or may not be associated with pneumo- developing countries, where hazardous pneumonitis. The clinical diagnosis of
coniotic nodules. This pattern of diffuse occupations like ship demolition and as- chronic hypersensitivity pneumonitis can
interstitial fibrosis appears to be associ- bestos milling are often poorly regu- be quite challenging because of the vari-
ated with a high prevalence of lung can- lated, the prevalence of asbestos-related ety of pulmonary presentations and the
cer, preferentially occurring in areas of disease on radiographs remains substan- diversity of potential antigenic causes,
lung fibrosis (107). tial (114,115). which may not be elicited in a routine
medical history (118).
Asbestos-related Lung and Pleural Disease Hypersensitivity Pneumonitis Imaging features of hypersensitivity
Though exposure to friable asbestos has Hypersensitivity pneumonitis is a group pneumonitis include poorly defined cen-
been increasingly regulated in developed of pulmonary syndromes caused by re- trilobular ground-glass nodules (Fig 15),

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STATE OF THE ART: Imaging of Occupational Lung Disease Cox et al
Figure 14  Figure 15  work­ers in 1992 was attributed to Acra-
Figure 14:  CT image through the right lower chest
in a subject with environmental exposure to vermic-
ulite contaminated with tremolite asbestos shows a
subtle noncalcified posterior pleural plaque (arrow).
ground-glass attenuation, mosaic atten-
uation, expiratory gas trapping, and
features of lung fibrosis, including retic-
ular abnormality and honeycombing
(119–124). Emphysema and cysts may
occur in chronic cases (62,77,125).
Classically, the presentation of hyper-
sensitivity pneu­ monitis has been di-
vided into acute, subacute, and chronic
forms. However, the imaging findings in
hypersensitivity pneumonitis do not
necessarily correlate with the duration
or presentation of symptoms, except
for the fact that fibrosis is found only in
chronic hypersensitivity pneumonitis
(Fig 16). When CT signs of lung fibrosis
are present, mortality is substantially
increased (126,127).
Chronic Beryllium Disease
Beryllium-related lung disease may be
acute (now very rare) or chronic. Al-
though chronic beryllium disease tech-
nically meets the definition of pneumo-
coniosis, it differs from pneumoconiosis
in the following ways: (a) It represents
a granulomatous hypersensitivity re-
sponse to inhaled beryllium, and (b)
its incidence and severity are not al-
ways related to the intensity and dura-
Radiology: Volume 270: Number 3—March 2014  n  radiology.rsna.org 691
Figure 15:  Thin-section CT image in a patient with
hypersensitivity pneumonitis demonstrates character-
istic diffuse ground-glass centrilobular opacities. Note
focal lobular areas of mosaic attenuation (arrows).
tion of exposure; in fact, it may occur
with relatively minimal exposure, par-
ticularly in those with a genetic predis-
position (128).
Exposure to beryllium occurs in a
variety of industries (including aero-
space, ceramics, dentistry, nuclear
weapons and reactors, and several
others) where workers may be at risk
for disease from either direct or indi-
rect exposure to the metal. Recently a
case series of community-acquired
chronic beryllium disease was report-
ed in a neighborhood surrounding a
beryllium manufacturing plant (68).
The radiographic and CT appear-
ances of chronic beryllium disease are
similar to those of sarcoidosis, though
mediastinal and hilar lymphadenopa-
thy are less common, occurring in
about 25% of cases (Fig 17) (129).
The radiologist should include the dif-
ferential diagnosis of chronic beryl-
lium disease in every patient with im-
aging appearances suggestive of
sarcoidosis. In a recent series of 84
patients with previously diagnosed
“sarcoidosis,” the diagnosis was cor-
rected to chronic beryllium disease in
34 (130).
Emergence of New Occupational Lung
Diseases
Industrial progress has resulted in mul-
tiple new causes of occupational lung
disease. Development of organizing
pneu­monia in a series of Spanish textile
min-FWN exposure and later termed
Ardystil syndrome (5,55,56,59). At the
Ardystil plant in Alcoy, Spain, aerosol-
ized Acramin-FWN for use in textile
printing resulted in inhalational expo-
sure of this product designed for brush
or sponge application. Romero et al
(56) found that nine of 14 Ardystil
syndrome patients demonstrated bilat-
eral, peripheral predominant, patchy
airspace consolidation on CT scans.
Exposure-related outbreaks have
also been reported related to the nylon
flocking, artificial flavoring, and flat-
panel screen industries. Initially recog-
nized at a Canadian plant in 1995,
flock worker’s lung arises from respi-
rable flock, an ultra-fine nylon fiber
used in the production of certain fab-
rics, and results in a nongranuloma-
tous interstitial lung disease (131).
Subsequently, eight workers at a dif-
ferent plant were diagnosed in 1998
with flock worker’s lung, characterized
on thin-section CT scans by patchy
ground-glass and consolidations or dif-
fuse micronodularity and at pathologic
evaluation by lymphocytic bronchiolitis
and peribronchiolitis with lymphoid
hyperplasia (15,16).
In 2000, eight workers at a micro-
wave popcorn plant in Missouri pre-
sented with constrictive bronchiolitis
associated with exposure to the artifi-
cial butter flavoring chemical, diacetyl
(2,3-butanedione), and termed flavor
worker’s lung (4,14).
Reports from Japan recognized the
relationship of indium-tin oxide to in-
terstitial lung disease (24,132). The
properties of indium-tin oxide allow for
production of transparent conductive
films utilized in flat-panel screens. Two
separate cases of indium-tin oxide ex-
posure were described related to the
flat-panel screen industry, both of
which resulted in biopsy-proved pulmo-
nary fibrosis. At CT imaging, the initial
case in 2002 resulted in subpleural hon-
eycombing, while the subsequent case
in 2003 demonstrated upper lobe pre-
dominant fine nodular opacities,
ground-glass opacities, and associated
emphysema. In 2010, Cummings et al
(12) described two additional cases of
STATE OF THE ART: Imaging of Occupational Lung Disease Cox et al

Figure 16  Figure 18 

Figure 18:  Thin-section CT image at the level of

Figure 16:  Thin-section CT images in a patient with fibrotic hypersensitivity pneumonitis. (a) Inspiratory the bronchus intermedius in a soldier with exertional
image demonstrates peripheral reticulation and traction bronchiectasis on a background of mosaic attenua- dyspnea following Middle East deployment shows
tion. (b) Expiratory image reveals areas of air trapping (arrowheads). diffuse ill-defined centrilobular nodules and back-
ground of mosaic attenuation consistent with small
airway disease.
Figure 17 
strictive bronchiolitis reported specific
exposure to combustion products from
an industrial sulfur fire in Mosul, Iraq.
The prevalence of and risk factors for
deployment-related lung disease await
further investigation. A multidisciplin-
ary group of scientists recently recom-
mended that postdeployment military
personnel with unexplained respira-
tory symptoms or physiologic impair-
Figure 17:  Thin-section CT images in a patient with occupational beryllium exposure. (a) At the level of ment should undergo diagnostic test-
the carina, perilymphatic nodularity due to chronic beryllium disease is present. Note associated bronchial ing including thin-section CT (133).
wall thickening (arrow) and background of mild mosaic attenuation. (b) Bone window demonstrates partial
calcification of mediastinal and hilar lymph nodes.
Conclusion
indium-tin oxide exposure resulting in copy, and pulmonary function testing The radiologist plays a pivotal role in
pulmonary alveolar proteinosis, with confirmed acute pulmonary toxicity, the diagnosis of occupational lung dis-
one resulting in death. which resolved without treatment. eases. Radiologic diagnosis of occupa-
Unregulated novel chemical agents Unique situations such as military tional lung disease requires awareness
may result in concentrated exposures service in a war zone may be associ- of the diverse patterns of lung injury
and acute respiratory illness. Lee et al ated with limited ability to control haz- related to occupational exposures, ap-
(13) reported 15 cases of 1,1-dichloro- ardous exposures and substantial vari- propriate use of CT, and awareness of
1-fluoroethane (HCFC-141b) exposure ability in occupational exposure risks. newer occupational exposures. The
resulting in acute pulmonary toxicity. In a case series by King et al (81), con- radiologist is often ideally placed to
Animal testing of HCFC-141b showed strictive bronchiolitis was described in recognize potential occupational lung
low risk for toxicity. However, when soldiers returning from Iraq and Af- disease and question the clinician
utilized in an electronics factory to ghanistan with symptoms of unex- about possible exposures that, if caus-
clean circuit boards in the setting of plained shortness of breath. While less ally relevant, may lead to more tar-
limited ventilation and no respiratory than a quarter of the soldiers demon- geted medical management and pre-
protection, HCFC-141b triggered on- strated abnormalities such as centri- vention.
set of respiratory symptoms in 15 lobular nodules or air-trapping on
workers over the course of 1 day. By thin-section CT scans (Fig 18), 38 out Disclosures of Conflicts of Interest: C.W.C. Fi-
the following day, all 15 workers pre- of 49 of those who underwent surgical nancial activities related to the present article:
none to disclose. Financial activities not related
sented to the hospital with progressive lung biopsy were diagnosed with con-
to the present article: Payment for lectures in-
respiratory symptoms. Subsequent strictive bronchiolitis. Many but not all cluding service on speakers’ bureaus for U.S.
evaluation with imaging, bronchos- of the soldiers diagnosed with con- Army Madigan AMC (one-time honorarium) and

692 radiology.rsna.org  n  Radiology: Volume 270: Number 3—March 2014

STATE OF THE ART: Imaging of Occupational Lung Disease Cox et al
Rocky Vista University (ongoing preclinical guest
lecturer). Other relationships: none to disclose.
C.S.R. Financial activities related to the present
article: Health Resources and Services Adminis-
tration (HRSA) grant, with some of author’s sal-
ary support for medical direction of Miners
Clinic of Colorado; support for travel to required
meetings for HRSA grant. Financial activities not
related to the present article: 1. Author provides
deposition testimony for patients seen in the oc-
cupational lung disease clinic. Fees for author’s
testimony are collected by the employer, Na-
tional Jewish Health, and are handled as clinical
revenue. No fees are paid to the author. 2. Au-
thor receives salary support from grants provid-
ing clinical services to coal and metal miners. 3.
Author’s grant travel expenses are paid for by
the HRSA grant. Other relationships: none to
disclose. D.A.L. Financial activities related to
the present article: none to disclose. Financial
activities not related to the present article: con-
sultancy to Perceptive Imaging, Inc, Intermune,
Inc, and Gilead, Inc; Author provide expert tes-
timony on flavor worker’s lung for Raphael
Metzger law firm (no fees); Grants/grants pend-
ing, Siemens, Inc. Other relationships: none to
disclose.
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