PNEUMOCONIOSIS

SGD B6
1. Janet Tee (1502005211)
2. Astari Rahayu Dewi (1502005084)
3. Anak Agung Istri Sarastriyani Dewi (1502005127)
4. I Gusti Ngurah Arya Nugraha (1502005259)
5. Hanina Mardhalillah (1502005180)
6. Made Dwi Satya Nugraha (1502005139)
7. Ronald Sugianto (1502005242)
8. Agilan Sethupathy (1502005210)
9. Shabrina Inderjit (1502005194)
10. Tifania Melucha Miguel Leong (1402005254)

FACULTY OF MEDICINE
UDAYANA UNIVERSITY
2017
CHAPTER I
BACKGROUND
1.1 Background
Occupational lung diseases are a broad group of diagnoses caused by the
inhalation of dusts, chemicals, or proteins, which then retained in the lung
parenchyma and inciting fibrosis. Pneumoconiosis is the term used for the
diseases associated with inhaling mineral dusts. The severity of the disease is
related to the material inhaled and the intensity and duration of the exposure.
Even individuals who do not work in the industry can develop occupational
disease through indirect exposure. Although these diseases have been
documented as far back as ancient Greece and Rome, the incidence of the
disease increased dramatically with the development of modern industry.1
Pneumoconiosis is defined for legal purposes as fibrosis of the lung due to
silica dust, asbestos or other dusts and includes the condition known as dust
reticulation. For medical purposes pneumoconiosis was described as the
presence of inhaled dust in the lungs and the non-neoplastic reaction to it.
Dusts that cause fibrosis are termed fibrogenic. It is important to differentiate
those dusts that provoke a fibrotic reaction in the lung, from those that are
retained without such a reaction. Silicosis, coal worker pneumoconiosis,
asbestosis, berylliosis and talcosis are examples of fibrotic pneumoconiosis.
Siderosis, stannosis and baritosis are non-fibrotic forms of pneumoconiosis
that result from inhalation of iron oxide, tin oxide, and barium sulfate
particles.1
Lately, many cases have been linked to environmental exposure to dust.
This suggests that pneumoconiosis is no more a pathology exclusively related
to work, cigarette smoking has a devastating impact of the health of dust-
exposed individuals. Rates of cigarette smoking as high as 80% have been
recorded among miners and other dust-exposed populations. Radiological
imaging plays an important role in the diagnosis of those occupational lung
diseases, including asbestos-related diseases, Silicosis and coal workers
pneumoconiosis.2
CHAPTER II

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 CONTENT

2.1 Definition
The pneumoconioses are a group of interstitial lung diseases caused by the
inhalation of certain dusts and the lung tissues reaction to the dust. The principal
cause of the pneumoconioses is work-place exposure; environmental exposures
have rarely given rise to these diseases.3
The primary pneumoconioses are asbestosis, silicosis, and coal workers
pneumoconiosis As their names imply, they are caused by inhalation of asbestos
fibers, silica dust, and coal mine dust. When severe, the diseases often lead to lung
impairment, disability, and premature death. From a public health perspective,
these conditions are entirely man-made, and can be avoided through appropriate
dust control.3
Other forms of pneumoconioses can be caused by inhaling dusts containing
aluminum, antimony, barium, graphite, iron, kaolin, mica, talc, among other dusts.
There is also a form called mixed-dust pneumoconiosis.3

2.2 Epidemiology
In 2013, it resulted in 260,000 deaths, up from 251,000 deaths in 1990. Of
these deaths, 46,000 were due to silicosis, 24,000 due to asbestosis and 25,000
due to coal workers pneumoconiosis.4
The prevalence of pneumoconiosis in American state on 1960 was about 30%
and this figure was significantly decreased in 2002 to only about 2.5%. The
prevalence of pneumoconiosis in UK were found as many as 265 cases for coal
miner pneumoconiosis and 40 other cases of pneumoconiosis. The prevalence of
pneumoconiosis in one industry in Indonesia period 1992 -2002 got the incidence
about 3.6%.5

2.3 Etiology and Classification

Occupational lung disorders can be classified based the biological properties
of the material inhaled, have been grouped into four main types: (i) disorders
caused by exposure to mineral (inorganic) dust; (ii) disorders caused by exposure

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 to gases and fumes; (iii) disorders caused by exposure to organic dust; (iv)
pulmonary and pleural malignancy caused by asbestos exposure leading to pleural
mesothelioma.6
Pneumoconiosis or occupational lung diseases are man-made in most cases,
resulting from inorganic dust exposure during mining, processing, or
manufacturing. Different exposures result in different diseases.7
These diseases classified based on the tissue reaction by the dust: pneumoconiosis
mimics/inert dust pneumoconiosis, uncomplicated pneumoconiosis, and
complicated pneumoconiosis. Further classification shown in table below.6

Table 1. Pneumoconiosis classification based on tissue reaction by the dust.1

Meanwhile there is other terminology traditional pneumoconiosis, which include

silicosis, coal workers pneumoconiosis, and asbestosis. Described as the most
common pneumoconiosis case occurred.
1. Silicosis
Silicosis is caused by exposure to free crystalline silica (SiO2),
occurs mainly in mines or foundries. The pathological hallmark is silicotic
nodules, which may often appear first in hillar or mediastinal lymph
nodes. The appearance of silicotic nodules may also be an important factor
in attributing an occupational etiology of bronchopulmonary cancer. The
absence of silicotic nodules should not necessarily exclude a diagnosis of
silica-induced lung disease. As long as there are routine exposure, further
diagnosis should be done if the clinical manifestation appears.8
2. Coal Workers Pneumoconiosis

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 Coal workers pneumoconiosis or black lung, caused by prolonged
exposure to respirable coal dust. The dust collects in the alveoli of the
lungs causing scarring of lung tissue, reduced elasticity of the lung, that
can seriously reduced the lung function. Coal workers pneumoconiosis
may or may not be associated with the presence of significant numbers of
silicotic nodule.8,9
3. Asbestosis
Asbestosis is a diffuse pulmonary fibrosis caused by inhalation of
excessive amounts of asbestos fibers. Pulmonary fibrosis of a particular
pattern and evidence of excess asbestos in the lungs must be present. The
term asbestosis should only be used to label the parenchymal disease
caused by asbestos exposure, and should not be used when only pleura
involved.8,10

2.4 Pathogenesis
The first factor for pathogenesis pneumoconiosis is particle dust and
respon body that specially in respiratory system. Pathogenesis of
pneumoconiosis is started from response alveolar macrofages to the dust that
enter to unit respiratory lung. There is phagocytosis of dust by macrophages
and the subsequent process is higly dependent on the toxity properties of dust
particles.11
The tissue reaction to the dust varies according to dust biological activity.
If the exposure, inorganic dust is long enough then the initial inflammatory
reaction develops. The main feature of this inflammation is the collection of
cells in the lower airway. Alveolitis may involve in the bronchioles and even
the large airways as they can cause injuries and fibrosis in the clinically
unknown alveolar units. Some dust like coal dust appears relatively inert and
accumulates in relatively large amounts in the lung with minimal tissue
reactions. Inert dust will remain in the macrophage until death by
macrophages due to age, then dust will come out and again phagocytosed by
other macrophages, macrophages with dust in it can migrate to the lymphoid
tissue or to the brochioles and is excreted throught the airways. In cytokoxic

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dust, macrophages-infected dust particles of the dust will cause the destruction
of macrophages followed by fibrositosis.11
According to Lipscomb, dust particles will stimulate the alveolar
macrophages to release products that mediate an inflammatory response and
begin the proliferation process of fibroblasts and collagen deposition. The
most common mediators involved in the pathogenesis of pneumoconiosis are
Tumor Necrosis Factor (TNF) , interleukin (IL) -6, IL-8, platelet derived
growth factor and transforming growth factor (TGF) . Most of these
mediators are essential for the process of fibrogenesis. An important
macrophage mediator responsible for tissue damage.11
Cytokines have been shown to play a role in the pathogenesis of
pneumoconiosis. Pappas summarizes the cytokines produced by alveolar
macrophages in response to dust particles entering the lungs which
subsequently cause fibrosis in the pulmonary interstitial tissues. This cytokine
consists of fibrogenesis factors such as TNF-, PDGF, IGF-1 and fibronectin
as well as proinflammatory factors such as LBT4, IL-8, IL-6, MIP1a.
Besides the process of dust phagocytosis by alveolar macrophages, more
important is the interstitialization of the dust particles. When dust particles
have been phagocytosed by macrophages then transferred to the mucosilier
system for the process of cleaning dust entering in the airway is categorized
successfully. The loss of epithelial integrity due to inflammatory mediators
released from alveolar macrophages is an early occurrence of fibrogenesis in
the pulmonary interstitial. When the dust particles have entered the interstitial,
the fate is determined by interstitial macrophages, phagocytosed to the
transferred of mediastinal lymph nodes or occurs chronic inflammatory
diuretic secretion on the interstitial.11
Cytokines released in interstitials such as PDGF, TGF, TNF, IL-1 cause
proliferation of fibroblasts and pneumococcal niosis. The properties of dust
toxicity determine the tissue reactions that occur in pneumoconiosis. Silica
and asbestos dust have a very strong biological effect. Parenchymal reactions
may be nodular fibrosis, a classic example of silicosis, diffuse fibrosis of
asbestosis and macular formation with focal emphysema due to coal dust.11

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 Figure 1. Pathogenesis of Pneumoconiosis11

2.5 Clinical Manifestation

Pneumoconiosis is one of a group of interstitial lung diseases caused by
breathing in certain kinds of dust particles that damage the lungs. It usually takes
years to develop. Because the lungs can't get rid of all these dust particles, they
cause inflammation in the lungs that can eventually lead to scar tissue.
Pneumoconiosis can be simple or complicated but for either simple or
complicated pneumoconiosis, the damage causes the loss of blood vessels and air
sacs in the lungs. The symptoms may include cough, loads of phlegm, shortness
of breath, tightness of chest, respiratory problems, cyanosis, bronchitis,
emphysema.12,13,14

2.6 Diagnosis
Diagnosis of pneumoconiosis cant be determined only with clinical
findings. A significant exposure of mineral dust that can cause pneumoconiosis
with a supporting latent period. Because of that, a thorough anamnesis about dust
level in working environment, duration of exposure, and use of protection gear is
absolutely needed. Some supporting test is needed to make the diagnosis more
accurate such as radiology imaging and pulmonary function test.15
2.6.1 Radiology Imaging
2.6.1.1 Chest X-Ray

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 The standard classification of International Labour Organization (ILO) is
used for the interpretation. In this test, small opacities are difficult to characterise.
The category of profusion is based on an assessment of opacities by comparison
with the standard radiographs. The category is determined by considering the
profusion throughout the affected zones of the lung and by comparing this with
the standard films. Even though this test can be used easily with a low cost
throughout the world, the sensitivity and specificity is practically low.16
2.6.1.2 Computed Tomography (CT) Scan
CT Scan is useful to estimate the level of fibrosis interstitial that happened,
size of emphysema, pleural change and to see if there are any necrosis or abscess
that come with the existing opacity on an individual. High Resolution CT (HRCT)
is more sensitive than conventional radiology to evaluate parenchyma
abnormalities on asbestosis, silicosis, and other pneumoconiosis. The most
common finding on pneumoconiosis with HRCT is nodular sentrilobular or high
attenuation on the branch area that looks similar to bronchiolar lesion. The typical
finding for silicosis, coal pneumoconiosis, and asbestosis with HRCT is a small
nodular opacities that predominant at upper lung. The small nodular opacities on
HRCT has two characteristics, ill-defined fine branching lines and well defined
discrete nodules. Asbestosis showed thickened line on intralobular and
interlobular, curvilinier and honeycomb, distributed predominantly at basal lung.16

2.6.2 Pulmonary Function Test

This test is done for diagnostic and epidemiologic purpose. Lung volume
examination with spirometer and diffuse capacity examination (DLco) need to be
done for this test. Normal result can be found on pneumoconiosis, but results that
showed obstruction, restriction, or mixed can be found also on pneumoconiosis.
Most of the diffuse lung disease caused by mineral dust is associated with
restriction abnormalities because there are fibrosis on lung parenchyma.
Inflammation, fibrosis, and distortion on respiratory tract that can lead to
respiratory tract obstruction can also be found on some condition.15
2.7 Differential Diagnosis
Hypertrophic pulmonary osteoarthropathy is a paraneoplastic syndrome seen
in patients with lung cancer. This condition is characterized by the presence of

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digital clubbing, periosteal thickening, synovial thickening, and severe pain of the
affected joints. 17,18
Idiopathic Pulmonary Fibrosis is a chronic, progressive form of fibrosis
(scarring) of the interstitium. Its cause is unknown. 17
Tuberculosis (TB) is caused by a bacterium called Mycobacterium
tuberculosis. The bacteria usually attack the lungs, but TB bacteria can attack any
part of the body such as the kidney, spine, and brain.17,19

2.8 Treatment
There is currently no cure for pneumoconiosis. Therefore, treatment and
management aids to control symptoms and preventing the disease from getting
even worse or developing others.20 It is necessary to take care of the heart and
lungs by maintaining a healthy lifestyle, getting adequate sleep, exercising
regularly and most importantly quitting smoking.20,21
Patients suffering pneumoconiosis are advised to avoid further exposure to the
mineral dust.20 Usage of an inhaler such as medications called bronchodilators
which open lung passages, or even oxygen therapy can be used to help lungs
function as well as possible.20,21 All patients should receive immunizations for
influenzae and pneumococci. Moreover, regular checkups should be made to help
spot any progression of pneumoconiosis.21

2.9 Prognosis
Prognosis is related to extent of fibrosis noted at diagnosis and past
cumulative exposure. Many patients with pneumoconiosis will not progress and
will go on to die from other conditions.22 The findings of the study show that the
long-term prognosis of patients with coal workers pneumoconiosis (CWP) after
acute respiratory failure (ARF) was poor even though a substantial proportion of
them could be weaned from the ventilator and discharged from the hospital.
Radiographic progressive massive fibrosis (PMF) was relatively common in CWP
with ARF, but its presence did not predict a poor ICU outcome. Radiographic
PMF was relatively common in patients with CWP and ARF receiving invasive
mechanical ventilator (MV) in the ICU, but its presence was not associated with

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the ICU mortality. Although a substantial proportion could be successfully weaned
from the ventilator and discharged from the hospital, the long-term prognosis was
poor.23

CHAPTER III
CONCLUSION

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 Pneumoconioses are a group of interstitial lung diseases caused by the
inhalation of certain dusts and the lung tissues reaction to the dust . The severity of
the disease is related to the material inhaled, intensity, and duration of the
exposure. The primary pneumoconioses are asbestosis, silicosis, and coal workers
pneumoconiosis. The principal cause is because of work-place exposure. In 2013,
it resulted in 260,000 deaths. Of those deaths, 46,000 were due to silicosis, 24,000
due to asbestosis, and 25,000 due to coal workers pneumoconiosis.
Pneumoconiosis usually takes years to develop, because the lungs can't get
rid of all these dust particles, they cause inflammation in the lungs that can
eventually lead to scar tissue. The damage causes the loss of blood vessels and air
sacs in the lungs. The symptoms may include cough, loads of phlegm, tightness of
chest, respiratory problems, and cyanosis.
Diagnosis of pneumoconiosis needs detailed anamnesis and supporting test
such as radiology imaging and pulmonary function test. It cannot be determined
only by the clinical findings because exposure of mineral dust that can cause
pneumoconiosis with a supporting latent period. The main differential diagnosis
are asbestosis, hypertrophic pulmonary osteoarthropathy, idiopathic pulmonary
fibrosis, silicosis, and tuberculosis.
There is currently no cure for pneumoconiosis. Treatment and
management aids to control symptoms and preventing the disease from getting
worse. Maintaining a healthy lifestyle, avoid further exposure to mineral dust,
usage of inhaler such as medications called bronchodilators can be used to help
lungs function well.
The long term prognosis was poor. Many patients with pneumoconiosis
will not progress and will go on to die from other conditions even though a
substantial proportion of the patient could be successfully weaned from the
ventilator and discharged from the hospital.

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