Chapter 57

Pneumoconiosis

Christopher J. Rees, Charles V. Pollack, Jr., and Victoria G. Riese

Name and Synonyms

Pneumoconiosis
Black Lung Disease (Coal Worker’s Pneumoconiosis)
Asbestosis
Silicosis

Incidence/Epidemiology

• The incidence of pneumoconiosis in Western nations has been declining for

the past 20 years. However, in developing nations, where regulatory oversight
is not as consistent, the incidence of these disorders continues to increase.
• From 1968 through 1992 in the United States, there were 100,800 death cer-
tificates listing pneumoconiosis as a contributing or primary cause of death.
• In 2013, there reportedly were about 250,000 deaths worldwide from
pneumoconiosis.
• The most common pneumoconioses are the result of exposure to coal dust,
silica, and asbestos.

C. J. Rees
Emergency Department, Pennsylvania Hospital, Philadelphia, PA, USA

C. V. Pollack, Jr. (*)
Department of Emergency Medicine, Thomas Jefferson University,
Philadelphia, PA, USA
V. G. Riese
Librarian Consultant, Eldersburg, MD, USA

© Springer Nature Switzerland AG 2019 819

C. V. Pollack, Jr. (ed.), Differential Diagnosis of Cardiopulmonary Disease,
https://doi.org/10.1007/978-3-319-63895-9_57
820 C. J. Rees et al.

Differential Diagnosis

• The differential diagnosis of pneumoconiosis is broad and includes the entire

spectrum of diseases that may present with cough and dyspnea, such as asthma,
chronic obstructive pulmonary disease (COPD), congestive heart failure (CHF),
pneumonia, lung cancer, and all the other interstitial lung diseases (ILDs).

Pathophysiology and Etiology

• Pneumoconioses are a group of ILDs caused by the chronic inhalation of

inorganic dusts.
• Pneumoconiosis classically refers only to dusts that cause a fibrotic, restric-
tive pattern of lung disease.
• Exposure to organic dusts tends to cause reactive airway disease that may
mimic asthma or, more chronically, obstructive diseases such as COPD.

Table Some types of pneumoconiosis according to dust and lung reaction

Inorganic Dust Type of Disease Lung Reaction
Asbestos Asbestosis Fibrosis
Silica (Quartz) Silicosis Fibrosis
Coal Coal Pneumoconiosis Fibrosis
Beryllium Beryllium Disease Fibrosis
Tungsten Carbide Hard Metal Disease Fibrosis
Iron Siderosis No Fibrosis
Tin Stannosis No Fibrosis
Barium Baritosis No Fibrosis
Organic Dust
Mouldy hay, straw and grain Farmer’s lung Fibrosis
Droppings and feathers Bird fancier’s lung Fibrosis
Mouldy sugar cane Bagassosis Fibrosis
Compost dust Mushroom worker’s lung No Fibrosis
Dust or mist Humidifier fever No Fibrosis
Dust of heat-treated sludge Sewage sludge disease No Fibrosis
Mould dust Cheese washers’ lung No Fibrosis
Dust of dander, hair particles, Animal handlers’ lung No Fibrosis
and dried urine of rats

Some types of pneumoconiosis according to dust and lung reaction [What are the
Effects of Dust on the Lungs?, http://www.ccohs.ca/oshanswers/chemicals/lungs_
dust.html, OSH Answers Fact Sheets, Canadian Centre for Occupational Health and
Safety (CCOHS), October 1, 2012. Reproduced with the permission of CCOHS,
2016.]
57 Pneumoconiosis 821

• Exposure to organic dusts also may cause a distinct syndrome: hypersensitiv-

ity pneumonitis.
• This discussion is limited to the classic pneumoconioses.
• The etiology of these diseases usually is multifactorial, with occupational and
environmental factors (such as exposure to cigarette smoke) interacting with
genetic risk to produce a spectrum of disease activity in affected individuals.
• Many different industries and metals may be associated with the development
of pneumoconiosis. This discussion centers on the three most common: coal
dust, silica, and asbestos.
• The exact pathophysiologic mechanisms by which these substances produce
fibrosis are not well elucidated. In general, it involves chronic immune activa-
tion due to direct exposure, phagocytosis of the inorganic particles by macro-
phages, and the generation of reactive oxygen species with subsequent
oxidative injury to the lung tissue.

Silicosis. “Dirty” macrophages in a subpleural perilymphatic and peribronchovas-

cular distribution associated with bronchiolocentric fibrotic nodules (haematoxy-
lin–eosin, ×20. Courtesy Dr Alberto Cavazza Reggio Emilia, Italy). [Spagnolo P,
Sverzellati N, Wells AU, Hansell DM. Imaging aspects of the diagnosis of sarcoid-
osis. Eur Radiol. 2014 Apr;24(4):807-16.] Caption from original
822 C. J. Rees et al.

Coronal section of the lower lobe in an insulator with asbestosis. There is coarse
linear interstitial fibrosis, but changes of advanced fibrosis or honeycombing are not
present. Note accompanying visceral pleural fibrosis [Sporn TA, Roggli
VL. Asbestosis. In: Oury TD, Sporn TA, Roggli VL, editors. Pathology of asbestos-­
associated diseases [Internet]. Berlin, Heidelberg: Springer; 2014 [cited 2015 Dec
22]. p.  53-80. Available from: http://link.springer.com/10.1007/978-3-642-41193-
9_4] Caption from original

Silicosis. There is a cuff of dust-filled histiocytes around a small bronchiole [Colby

TV, Leslie KO. Pathology of diffuse lung disease. In: Baughman RP, du Bois RM,
editors. Diffuse lung disease [Internet]. New York: Springer; 2012 [cited 2016 Jan
14]. p.  49-70. Available from: http://link.springer.com/10.1007/978-1-4419-9771-
5_4] Caption from original
57 Pneumoconiosis 823

• Coal dust: Coal is a combustible rock formed over eons by the biologic and
geologic processing of dead plant matter. Coal is considered a fossil fuel, and
the burning of coal is the largest source of energy for electricity generation
worldwide. Long-term exposure (>10–20 years) to coal dust in coal mines
may cause coal worker’s pneumoconiosis (CWP). Inhaled coal dust appears
to become phagocytized by macrophages, which tend to group together and
develop into “coal macules” within the lung tissue. CWP may be classified
radiographically and clinically into simple or complicated CWP.  Cigarette
smoking does not appear to increase the incidence of CWP.
• Simple CWP is diagnosed when coal macules grow to about 2–5 mm and
become visible on plain chest x-ray (CXR; within upper lung zones).
These patients usually are asymptomatic. Simple CWP may be seen in
about 10–15 % of coal miners who have worked in the mines for 20 years
or more.

Coal workers pneumoconiosis. HRCT at the level of the upper lobes exhibits a “nodu-
lar without tree-in-bud pattern” characterized by ill-defined centrilobular nodules of
slightly variable size that have an upper lobe and posterior predominance. A distinc-
tive characteristic occasionally observed is that the micronodules of CWP tend to be
less sharply defined and of more granular density than those of silicosis. [From article:
Mimics in chest disease: interstitial opacities. Insights Imaging. 2013 Feb;4(1):9-27.
https://doi.org/10.1007/s13244-012-0207-7, at http://link.springer.com/article/10.100
7%2Fs13244-012-0207-7; by Anastasia Oikonomou, Panos Prassopoulos, © The
Author(s) 2012; licensed under Creative Commons Attribution License http://cre-
ativecommons.org/licenses/by/2.0] Caption and text from original
824 C. J. Rees et al.

• Complicated CWP is diagnosed when these macules coalesce into nodules

1 cm or larger. These nodules may take up an entire lobe. These patients usually
have symptoms of dyspnea and chronic cough with a restrictive physiology.
When the macules become very large and associated with fibrosis, the term
progressive massive fibrosis (PMF) may be applied. This also is often referred
to as “black lung”. These patients have severe symptoms associated with
hypoxia and a high ­mortality rate.

Coal worker’s pneumoconiosis. PA chest film: This study demonstrates progressive

massive fibrosis, which is usually seen in the upper lobes and posterior to midline
on lateral view. Peripheral to the masses is lucency, also very characteristic as the
masses “migrate” toward the hila [Goodman PC. Radiography and CT of occupa-
tional and environmental lung diseases. In: Huang Y-CT, Ghio AJ, Maier LA, edi-
tors. A clinical guide to occupational and environmental lung diseases [Internet].
Totowa, NJ: Humana Press; 2012 [cited 2015 Dec 22]. p. 59-92. Available from:
http://link.springer.com/10.1007/978-1-62703-149-3_4] Caption from original
• Silica: Free silica (silicon dioxide, SiO2, crystalline quartz) is commonly
encountered by employees in the mining, stonecutting, cement manufactur-
ing, and other stone-related industries. In general, many years of exposure are
required to develop pulmonary fibrosis. Silicosis also may be classified as
simple or complicated. There also is a much less common syndrome from
acute, high-intensity exposure: acute silicosis. Silica is taken up by alveolar
macrophages, to which it is toxic. Patients with silicosis therefore have an
increased risk for atypical lung infections associated with decreased macro-
phage function, such as tuberculosis, atypical mycobacteria, and fungi.
• Simple silicosis, like simple CWP, is marked by the appearance on CXR of
small (0.3–5-mm) round opacities in the upper lobes. These patients are
mostly asymptomatic. About 20 % of patients will have associated calcifi-
cation of their hilar lymph nodes, which gives a characteristic “eggshell”
appearance on CXR and high-resolution CT (HRCT).
57 Pneumoconiosis 825

Silicotic nodules. (a) Centrilobular and randomly distributed pleural nodules and
large opacity (arrow) due to complicated silicosis (progressive massive fibrosis). (b)
Egg-shell calcification (arrow) in lymph nodes. [Hering KG. Pneumoconioses. In:
Baert AL, editor. Encyclopedia of diagnostic imaging [Internet]. Berlin, Heidelberg:
Springer; 2008 [cited 2015 Dec 22]. p. 1509-12. Available from: http://www.spring-
erlink.com/index/10.1007/978-3-540-35280-8_1976] Caption from original

Silicosis. PA chest film demonstrates bilateral small nodules seen best over the lin-
gual. [Goodman PC. Radiography and CT of occupational and environmental lung
diseases. In: Huang Y-CT, Ghio AJ, Maier LA, editors. A clinical guide to occupa-
tional and environmental lung diseases [Internet]. Totowa, NJ: Humana Press; 2012
[cited 2015 Dec 22]. p. 59-92. Available from: http://link.springer.com/10.1007/978-
1-62703-149-3_4] Caption from original
• Complicated silicosis occurs when the nodules grow or coalesce to greater
than 1 cm in diameter. This usually is associated with significant fibrosis and
usually leads to symptoms. As in CWP, these fibrotic nodules may become
quite large and also lead to PMF and significant functional impairment and
mortality. Once the process of fibrosis starts, it may continue even in the
absence of continued exposure.
826 C. J. Rees et al.

Silicosis. Single slice from a CT scan in lung windows demonstrates the typical
upper posterior location of conglomerate opacities or progressive massive fibrosis
in a patient with silicosis. Note the small clustered nodules posterior to the right-­
sided PMF as well as the bilateral hilar and mediastinal calcified lymph nodes. Also
note that some calcified parenchymal nodules are incorporated in the PMF.
[Goodman PC. Radiography and CT of occupational and environmental lung dis-
eases. In: Huang Y-CT, Ghio AJ, Maier LA, editors. A clinical guide to occupational
and environmental lung diseases [Internet]. Totowa, NJ: Humana Press; 2012 [cited
2015 Dec 22]. p.  59-92. Available from: http://link.springer.com/10.1007/978-1-
62703-149-3_4] Caption from original
• Acute silicosis is an uncommon syndrome that occurs after short-term expo-
sure (about 1 year) to high concentrations of silica in confined spaces (e.g.,
from sandblasting or tunneling through rock with a high quartz content). It is
manifest with progressive dyspnea and a chronic, usually nonproductive
cough, although the patient occasionally may have gelatinous sputum, with
low-grade fever and constitutional symptoms. CXR usually reveals a diffuse
miliary pattern but may show diffuse alveolar opacities. HRCT shows a char-
acteristic “crazy paving” pattern.
• Asbestos: Asbestos is a general term that refers to several mineral silicates.
Silicate minerals are the predominant minerals in rock and make up 90 % of the
earth’s crust. These silicates differ from silica, which is silicon dioxide; rather,
silicates have many different ratios of silicon to oxygen. Asbestos is character-
ized by being made up of long, thin, fiber-like crystals. Each visible fiber is
composed of millions of microscopic “fibrils” that may be released by abrasion
and other processes. Asbestos has been mined and used for millennia. It has
excellent thermal, electrical, and acoustic insulating properties and is markedly
fire resistant. Although synthetic materials largely have replaced asbestos use in
developed nations, asbestos continues to be mined and used widely in develop-
ing countries. Asbestos predominantly affects the respiratory tract and causes
pleural fibrosis, pulmonary fibrosis, cancers of the respiratory tract, and pleural
and pulmonary mesothelioma. The development of asbestos-related diseases is
57 Pneumoconiosis 827

directly related to the extent and duration of exposure. In general, more than 10
years of exposure is necessary for any of these diseases to develop.
• Asbestosis is the term given to the pneumoconiosis associated with asbes-
tos exposure. It is a diffuse, nodular, interstitial fibrosing disease of the
lung. CXR usually shows the typical progression of disease, usually with
pleural plaques as the initial finding. These plaques are observed as thick-
ening or calcification of the parietal pleura, usually along the diaphrag-
matic border. Pleural plaques are a clue to significant asbestos exposure;
they generally are asymptomatic and in isolation do not signify underlying
pulmonary disease. Benign pleural effusions also may occur. As the disease
progresses, CXR will show linear opacities in the lung bases that may
become irregularly shaped and spread into the middle and upper lung
zones. Severe disease may be associated with a diffuse ground-glass
appearance and/or honeycombing on CXR. Once patients become symp-
tomatic, they demonstrate restrictive pulmonary disease with decreased
lung volumes and decreased diffusing capacity.

Asbestosis and asbestos-related pleural plaques. PA chest film demonstrates bibasi-

lar heterogeneous irregular lung opacities (look at lung overlying both costophrenic
angles) as well as calcified bilateral pleural plaques, many seen en face, which
makes assessment of underlying lung disease difficult [Goodman PC. Radiography
and CT of occupational and environmental lung diseases. In: Huang Y-CT, Ghio AJ,
Maier LA, editors. A clinical guide to occupational and ­environmental lung diseases
[Internet]. Totowa, NJ: Humana Press; 2012 [cited 2015 Dec 22]. p. 59-92. Available
from: http://link.springer.com/10.1007/978-1-62703-149-3_4] Caption from
original
• Other asbestos-related pulmonary disease:
• Lung cancer is the most common cancer associated with asbestos expo-
sure. It is directly related to the extent and duration of the exposure.
828 C. J. Rees et al.

Smoking dramatically increases the risk of lung cancer in those exposed to

asbestos. The risk is beyond what would be expected from just adding each
risk (asbestos exposure and smoking) individually.
• Mesothelioma. Pleural and peritoneal mesothelioma is associated with
asbestos exposure. It may occur with much less exposure and with pro-
longed latent periods (up to 40 years). Smoking does not appear to increase
the risk of mesothelioma. Mesothelioma is much less common than lung
cancer.

Presentation

Typical/“Classic”

• Pneumoconiosis may range from asymptomatic findings on imaging to severe,

life-threatening restrictive pulmonary disease.
• Patients who develop symptoms usually will have slowly progressive short-
ness of breath and a dry cough.
• It usually is possible to obtain a history of occupational exposure to a known
cause of pneumoconiosis.
• On examination, symptomatic patients usually have fine, inspiratory
crackles.
• CXR and/or HRCT of the lungs usually show the typical changes of the incit-
ing pneumoconiosis (see “Imaging”).

Atypical

• Silicosis rarely may present more acutely, in patients who have been exposed
to large amounts of silica dust in a small space (such as in tunneling and sand-
blasting). Acute silicosis may occur with short-term exposure (1 year or less).
The presentation of acute silicosis is unlike that of usual silicosis (or other
pneumoconioses), as it is not a restrictive disease. Although patients with
acute silicosis have shortness of breath and cough, the cough may produce a
copious amount of thick, white sputum. CXR may show diffuse, miliary nod-
ules that subsequently develop into lobar consolidations. HRCT reveals the
characteristic crazy-paving appearance of the lung parenchyma.
57 Pneumoconiosis 829

Primary Differential Considerations

• Pneumonia
• Acute exacerbation of COPD
• Pulmonary edema
• Acute exacerbation of asthma
• Lung cancer

History and Physical Exam

Findings That Confirm Diagnosis

• The diagnosis often may be nearly confirmed by a history of prolonged occu-

pational exposure to a known inciting agent.
• There are no pathognomic physical examination findings for pneumoconio-
sis. Patients often demonstrate the signs of restrictive lung disease, such as
diffuse, fine inspiratory crackles. Later findings with more advanced disease
may include digital clubbing and hypoxia.
• The aforementioned findings together with a confirmatory imaging study con-
firm the diagnosis.

Factors That Suggest Diagnosis

• A history of occupational exposure to a known inciting agent should suggest

the diagnosis.
• Symptoms that occur, or worsen, only while the patient is at work strongly
suggest an occupational cause.

Factors That Exclude Diagnosis

• The complete lack of any occupational/environmental/hobby exposure to any

of the known inciting agents for pneumoconiosis should lead to evaluation for
an alternative diagnosis.
830 C. J. Rees et al.

Ancillary Studies

Pulmonary Function Studies

• Pulmonary function tests (PFTs) may be very helpful in the diagnosis of

pneumoconiosis. PFTs should show a restrictive pattern, with diffusely
decreased lung volumes (total lung capacity [TLC], functional residual capac-
ity [FRC], residual volume [RV], and forced vital capacity [FVC]) and a
decreased diffusing capacity for carbon monoxide (DLCO). As opposed to
obstructive lung disease (asthma, COPD), airway resistance in restrictive lung
disease is normal.

Laboratory

• There are no laboratory studies particularly helpful for the diagnosis or man-
agement of pneumoconiosis.

Imaging

• CXR:
• The plain CXR may be extremely useful in the diagnosis of
pneumoconiosis.
• In general, small round opacities in the upper lung zones are characteristic
of both simple silicosis and simple CWP.
• In both silicosis and CWP, the nodules may coalesce and grow to 1 cm or
greater. Both diseases also progress to significant pulmonary fibrosis with
larger areas of opacity as well as lung volume loss, usually noted in the
upper lung zones. Sometimes these changes involve an entire lobe or even
multiple lobes; this situation is termed progressive massive fibrosis.
• About 20 % of patients with silicosis will develop calcification of the hilar
lymph nodes, as seen on CXR; this is termed eggshell calcification and is
characteristic of silicosis.
• Asbestosis is characterized by pleural plaques (usually diaphragmatic) and
small linear opacities in the lung bases. These opacities may spread to
include all lung fields.
• HRCT of the lungs:
57 Pneumoconiosis 831

• HRCT is very helpful in the diagnosis and evaluation of all the ILDs.
• The changes associated with these diseases may be appreciated earlier and
be more characteristic on HRCT as compared with CXR.
• HCRT has been shown to improve the detection and diagnosis of asbesto-
sis compared with plain CXR.

HRCT scan of a 62 year old plumber with asbestosis showing linear opacities and
subpleural nodular opacities (upper left), ground-glass attenuation, subpleural hon-
eycombing, and calcified plaques [Müller-Quernheim J, Zissel G, Kayser G, Prasse
A.  Chronic beryllium disease and other interstitial lung diseases of occupational
origin. In: Cottin V, Cordier J-F, Richeldi L, editors. Orphan lung diseases [Internet].
London: Springer; 2015 [cited 2015 Dec 22]. p. 473-91. Available from: http://link.
springer.com/10.1007/978-1-4471-2401-6_30] Caption from original
832 C. J. Rees et al.

• HRCT may lead to consideration of alternative ILDs in the differential

diagnosis.
• HRCT may demonstrate the crazy-paving pattern typical of acute silicosis.

Coal worker’s pneumoconiosis. Single slice of a CT scan demonstrates progressive

massive fibrosis as represented by the larger opacities posterior to midline in the
upper lobes. Just adjacent to the masses are very small nodular opacities which
represent the earlier changes of coal worker’s pneumoconiosis. As these small nod-
ules coalesce, the large opacities are formed. As the masses migrate centrally, areas
of emphysema are formed in the lung periphery as seen here bilaterally [Goodman
PC.  Radiography and CT of occupational and environmental lung diseases. In:
Huang Y-CT, Ghio AJ, Maier LA, editors. A clinical guide to occupational and envi-
ronmental lung diseases [Internet]. Totowa, NJ: Humana Press; 2012 [cited 2015
Dec 22]. p. 59-92. Available from: http://link.springer.com/10.1007/978-1-62703-
149-3_4] Caption adapted from original

Special Populations

Age

• Given the decades-long latency between exposure and disease, these are dis-
eases of middle-aged to older adults.

Co-morbidities

• There are multiple comorbidities of importance. Many of these patients also

have risk factors for other pulmonary diseases, such as COPD, from other
exposures and smoking, making the diagnosis and management more
difficult.
57 Pneumoconiosis 833

• In many patients, the etiology of their pulmonary disease is multifactorial and

includes occupational, environmental (smoking, air pollution), and genetic
factors.
• Any cause of chronic dyspnea and cough (COPD, CHF, another ILD) may
coexist with a pneumoconiosis.
• Patients with silicosis have decreased alveolar macrophage numbers and
function, because silica is cytotoxic to these macrophages. These patients
then have an increased risk and incidence of pulmonary infections associated
with decreased macrophage function, primarily tuberculosis, atypical myco-
bacterial pneumonia, and fungal pneumonia.
• Silicosis (and to a lesser extent, CWP) also is associated with an increased
incidence of autoimmune connective tissue diseases, such as rheumatoid
arthritis (both silicosis and CWP) and scleroderma (silicosis only).
Seropositive rheumatoid arthritis associated with findings of simple silicosis
or simple CWP on CXR has been called Caplan’s syndrome.

Pitfalls in Diagnosis

Critical Steps Not to Miss

• It is critical to obtain a complete occupational, environmental, and hobby

history to be able to ascertain any significant exposures the patient may have
sustained.
• If supported by the history, and the diagnosis is being considered, it is criti-
cal to perform appropriate imaging (CXR, HRCT) and PFTs to secure the
diagnosis.

Mimics

• Many different diseases may present similarly to pneumoconiosis (with dys-

pnea and cough), including all the ILDs, COPD, asthma, and CHF.
• With an appropriate history, examination, imaging, and PFTs, the mimics
include other restrictive lung diseases, such as other ILDs.

Time-Dependent Interventions

• These disorders tend to be chronic and slowly progressive, so there are no

significant time-dependent interventions.
834 C. J. Rees et al.

• If a patient presents with hypoxia, oxygen should be administered.

• If a patient is having ventilatory difficulty, ventilation should be supported.
Patients with ventilatory difficulty generally have advanced disease, and the
approach to managing ventilatory emergencies would ideally have been dis-
cussed with the patient and family and decisions made before the acute event.

Overall Principles of Treatment

• There is no specific treatment for any pneumoconiosis.

• Treatment tends to be supportive and should proceed as for most restrictive
lung diseases.
• Patients with hypoxia require oxygen.
• Patients with silicosis should be monitored for atypical lung infections, such
as tuberculosis.
• All patients should receive routine care as appropriate for any patient with
chronic lung disease, including appropriate vaccinations (influenza,
pneumococcus).
• Patients who smoke tobacco should be offered all assistance needed to stop.
• Patients still working in an occupation with risk for continued exposure
should stop or be moved to a position with no exposure risk.
• These patients may be at increased risk for lung cancer and may need periodic
monitoring.

Disease Course

• These diseases are slowly progressive.

• The diseases may continue to progress even after the exposure has stopped.
• There is a large individual variation in the severity of disease. Although devel-
opment of a pneumoconiosis is related to the extent and duration of exposure,
severity of disease is less so.
• Many patients will remain asymptomatic, with only CXR findings, through-
out their lives. Some patients may develop only minor symptoms; others may
progress to life-altering and -shortening disease.

Related Evidence

Papers of particular interest have been highlighted as:

** Of key importance
57 Pneumoconiosis 835

Review

Prazakova S, Thomas PS, Sandrini A, Yates DH. Asbestos and the lung in the 21st
century: an update. Clin Respir J. 2014 Jan;8(1):1-10. https://doi.org/10.1111/
crj.12028. PMID: 23711077. http://www.ncbi.nlm.nih.gov/pubmed/23711077 **
Jun JS, Jung JI, Kim HR, Ahn MI, Han DH, Ko JM, Park SH, Lee HG, Arakawa H,
Koo JW. Complications of pneumoconiosis: radiologic overview. Eur J Radiol.
2013 Oct;82(10):1819-30. https://doi.org/10.1016/j.ejrad.2013.05.026. PMID:
23791520. http://www.ncbi.nlm.nih.gov/pubmed/23791520 **
Cullinan P, Reid P. Pneumoconiosis. Prim Care Respir J. 2013 Jun;22(2):249-52.
https://doi.org/10.4104/pcrj.2013.00055. PMID: 23708110. http://www.ncbi.
nlm.nih.gov/pubmed/23708110 **
Karkhanis VS, Joshi JM.  Pneumoconioses. Indian J Chest Dis Allied Sci. 2013
Jan-Mar;55(1):25-34. PMID: 23798087. http://www.ncbi.nlm.nih.gov/pubmed/
23798087 **
Laney AS, Weissman DN. The classic pneumoconioses: new epidemiological and
laboratory observations. Clin Chest Med. 2012 Dec;33(4):745-58. https://doi.
org/10.1016/j.ccm.2012.08.005. PMID: 23153613. http://www.ncbi.nlm.nih.
gov/pubmed/23153613 **
Leung CC, Yu IT, Chen W.  Silicosis. Lancet. 2012 May 26;379(9830):2008-18.
https://doi.org/10.1016/S0140-6736(12)60235-9. PMID: 22534002. http://www.
ncbi.nlm.nih.gov/pubmed/22534002 **
Review. Yucesoy B, Luster MI. Genetic susceptibility in pneumoconiosis. Toxicol
Lett. 2007 Feb 5;168(3):249-54. PMID: 17161563. http://www.ncbi.nlm.nih.
gov/pubmed/17161563 **

Use PubMed Clinical Queries to find the most recent evidence. Use this search
strategy:
“Pneumoconiosis”[Mesh] OR “Pneumoconiosis”