SILICOSIS

S I L I C O S I S
Dr. RAVEENDRA REDDY.K
 DEFINITION
• Fibrosing disease of lungs caused by
inhalation, retention and pulmonary reaction
to Crystalline silica.
• Occupational lung disease attributable to
inhalation of silicon dioxide, commonly known
as silica, in crystalline form usually as quartz
•Silicon dioxide, or silica, is the earth’s most abundant mineral.

•Silicosis occur when workers are consistently exposed to silica

particles of respirable size (0.5–5.0 μm in diameter) at levels
exceeding those recognized to be safe.
 FREE : 1.quartz (including granite)
2.flint
3.opal
4.diatomite.

SILICA
(silicon dioxide)

Combined (silicates) :1.asbestos

2.talc
3.kaolin
 Crystalline form: 1. quartz (in sand and many rocks)

2.Cristobalite
3.Tridymite
SILICA naturally in lava and
4.Coesite formed by the heating
of quartz or amorphous
5.Shistovite silica.

Amorphous 1.Diatomite (skeletons of marine organisms)

2.Vitreous silica (glass)

Crystalline form silica are different in their structure, fibrogenicity,

and biologic activity.
Amorphous silica is relatively less fibrogenic and does not cause
lung fibrosis.
Bronchitis, a well-recognized effect of chronic dust
inhalation, can occur with silica dust inhalation.

Silica exposure can be associated with:

Scleroderma
1.Autoimmune diseases :
SLE
2.Nephropathy
RA
3.Tuberculosis
4.lung cancer
Major industries with silica exposure
silicosis, is caused by the inhalation of respirable
size silica particles, and can be categorized by recognizable
findings on the chest radiograph.

Silicosis generally requires prolonged exposure to

respirable crystalline free silica at levels exceeding normal
standards.

Most forms of silicosis develop slowly,Usually 10 to 30

years are required from the beginning of exposure to the onset
of clinical manifestations.
 Most important factors include:

1. Silica dust concentration in the air,

2. Duration of dust exposure,
3. Crystalline structure of the silica
4. Percent of free silica,
5. Particle size.

host factors such as genetics, smoking, and underlying

diseases may play a part in the development of silicosis.
 Classification of silicosis
simple
-chronic or classic
>15 yrs PMF
- accelerated
SILICOSIS
5 to 10 yrs
- acute
up to 5 yrs
*PMF– complicated or conglomerate silicosis
{Progressive massive fibrosis}
 CLASSIC SILICOSIS

Ranging from simple silicosis (presenting as nodular

pulmonary fibrosis with or without symptoms) to progressive
massive fibrosis (severely disabling restrictive lung disease).

These features usually develop slowly and frequently require

a working lifetime to develop.
 CLASSIC SILICOSIS
in a small percentage of workers, the radiographic features
of simple silicosis lead to progressive massive fibrosis in less
than 10 years (accelerated Silicosis )

Development of these radiographic features so soon after

beginning exposure to silica means that progre- ssion of
disease and severe respiratory impairment is very likely to
occur.
 Diagnosis
There are three requirements for the diagnosis of silicosis:

1.History of silica exposure sufficient

to cause illness.
2. Chest radiograph features consistent
with silicosis.
3. Absence of other illnesses that mimic
silicosis.

Other chest illnesses : rheumatoid nodules, tumor,

infection, other pneumoconiosis, or sarcoidosis
 Pathogenesis and histologic features
of classic silicosis
Particles less than 5.0 μm in diameter are depo sited in the
alveoli, most often in the upper lung zones.
Particles less than 1.0 μm in diameter are believed to be
the most fibrogenic and most able to penetrate into the
interstitium.
Inhaled silica particles interact with alveolar macrophages
and other lung cells in a complex cascade of events resulting
in lung inflammation, fibrosis, and tissue remodeling
forming silicotic nodules.
This nodule usually forms near the small bronchioles.

In some workers with relatively low silica exposure, inhaled

silica is cleared from the lung and deposited in
the lymph nodes and presentation of calcified regional hilar
lymph nodes on the chest radiograph may
be noted without an extensive background of small
rounded opacities.

In microscopic view nodules are onion skin-like pattern

Photomicrograph (230×) of a well-developed silicotic nodule, with central
hyalinization and concentrically arranged collagen fibers providing the onion-skin
appearance. Peripherally, a rim of dust containing macrophages is seen.
 Simple silicosis
Usually do not have chest symptoms.

Some, however, report a chronic productive cough,

a feature likely similar to industrial bronchitis from
dust exposure.

Physical examination of the chest usually is unrem-

arkable; audible coarse sounds are the result of
coexisting bronchitis.

Roentgenographically, simple silicosis typically

appears as an upper zone distribution of rounded
opacities less than 1 cm in diameter.
This PA chest
radiograph is taken
from a 24-year-old
worker employed for
5 years as a bagger
in the production of
silica flour.
Small rounded
opacities (ILO 2/2)
are diffusely present
in both mid- and
upper zones,
consistent with
simple silicosis.
Hilar lymph nodes are often enlarged with a
distinctive peripheral calcification, described as
eggshell calcification.
High-resolution CT scans have been to shown to have a
good correlation with the nodular findings of silicosis on the
chest radiograph, and a better description of the extent of
emphysema compared to the chest radiograph.

Correlation between lung function tests and the chest

radiograph and CT scan is variable.

PFT in simple silicosis may be a trend for values to

progress toward airways obstruction.
 Progressive massive fibrosis
 Is the result of the conglomeration of small rounded
opacities.

 It has been traditionally recognized that progressive

massive fibrosis develops on a
background of advanced simple silicosis.

 However, not all PMF patients have an advanced

degree of simple coal workers’ pneumoconiosis
 symptoms
 The respiratory symptoms can be variable; ranging
from only a chronic productive cough
to exertional dyspnea and, in some persons, ultimately
to respiratory failure.
 Physical examination
 Physical examination demonstrates decreased breath
sounds, and if the illness is extensive, signs of cor-
pulmonale and impending respiratory failure.

 Crackles usually are not audible, and clubbing, if

present, is attributable to another cause.
 CXR
 Nodules >1 cm in diameter on a background of small rounded
opacities characteristic of simple silicosis:

- begins peripherally and migrates centrally

- prominently in the upper lobes .

 As these fibrous masses in the upper lobe progressively enlarge,

the hila are retracted upward and the lower zones become
hyperinflated and appear emphysematous
 PFT
 Initially demonstrate a decrease incompli-
ance, followed by decreases in lung volumes and
diffusing capacity.

 If bronchial distortion and lower zone hyper- inflation

are present, the forced expiratory time is likely to be
prolonged and airflow obstruction is measurable.
 Accelerated silicosis
Accelerated silicosis is characterized by the same features as
classic silicosis except that the time from
initial exposure to silica to the development of radio- graphic
changes and ensuing respiratory impairment
is much shorter.

The chest radiograph may demonstrate rounded opacities as early

as 4 years after initial silica exposure.

Result of exposure to grossly excessive levels of dust.

Rapid progression to progressive massive fibrosis is associated

with severe respiratory impairment.
 Acute silicosis
 After a short duration of exposure to a high concentra- tions of
respirable free silica.

 The worker has a relatively rapid onset of chest symptoms and

progressive respiratory impairment.

 Deaths of a large number of these workers occurred within a

year after the onset of symptoms.
 Acute silicosis
•Cough

•Weight loss

•Fatigue

1-3 years •Pleuretic pain 1 year

Initial Death
Exposure •Crackles

•Cyanosis

•Cor pulmonale

•Respiratory failure

symptoms occurring less than a year after beginning sandblasting have been
reported.
 ASSOCIATED ILLNESSES

• Mycobacterial infections
• Carcinoma of the lung
• Connective tissue disease
• Renal and extra pulmonary involvement
 Mycobacterial infection
 Silica particles increase the susceptibility to mycobacterial
infection by altering cell mediated immunity.
 The incidence of tuberculosis is likely to be greater in workers
with accelerated or acute silicosis.
 Silica exposure, by itself and in the absence of silicosis, is a risk
factor for tuberculosis.
 The frequency of mycobacterial infection increase as the extent
of radiographic changes.
 Silica exposure can impress on mortality in T.B patients.( 4
years earlier)
 Mycobacterial infection
The diagnosis of tuberculosis in workers with silicosis
sometimes can be difficult Because :

1. tuberculous infections can be walled off in the lung by silica-

induced fibrosis.
2. A false-negative acid-fast-staining sputum smear may occasionally
be present.
3. Constitutional symptoms, such as fatigue, fever, dyspnea, and
weight loss, can be seen in workers with worsening silicosis
independent of a mycobacterial infection.
4. Finally, the radiographic changes of tuberculosis may mimic
advanced silicosis.
 Mycobacterial infection

 The combination of silicosis and tuberculosis is more difficult

to treat.

 Those with silicosis should undergo regular PPD skin

testing.
When you doubt to T.B in a silicotic
worker?
Radiographic progression over a short time period.

Coalescence of nodules in the upper lung fields, or

cavitation of a pre-existing lesion .
 Carcinoma of lung
(IARC) concluded that there is sufficient evidence to
judge silica a carcinogen
for humans.

 The risk of lung cancer is highest in workers with

silicosis who also smoke.

 The risk in those exposed to silica but without

silicosis is less clear.
 Connective tissue disease
 A number of studies demonstrate increased rates of
arthritis, scleroderma, rheumatoid arthritis,
musculoskeletal disease, and renal insufficiency in
silica exposed populations.

 workers with dust exposure and rheumatoid arthritis

upper zone peripheral nodules appeared more
frequently in the lungs . This presentation of
rheumatoid nodules in workers with silica exposure
has been termed Caplan’s syndrome.
 Renal & extra pulmonary involvement

• Renal disease has been attributed both to a toxic

effect or silica or an immunologically mediated
process.

• Silicotic lesions have also been described in the liver ,

spleen, bone marrow, and remote lymph nodes. ( the
result of lymphatic or hematogenous spread )
 Prevention & management

 Product substitution of silica with less toxic particles

in abrasive blasting.

 Control of air-borne dust concentration

through engineering interventions.

 Appropriate use of respiratory protective devices.

 Prevention & management
Medical screening of silica-exposed workers
is generally recommended, using

questionnaires
chest x-rays
spirometry.
And….PPD
 Prevention & management

 in countries with a high endemic rate of tuberculosis,

yearly testing and if TB is
less frequent, less frequent testing would
be appropriate.

 With a PPD+ test without clinical evidence of

active tuberculosis, at least 1 year of Isoniazid
therapy is indicated.
 Prevention & management
 The rate of FEV1 and FVC decline increased with
profusion of opacities.
 According to one study:

Decline in FEV1 at Decline in FEC at

year year

silica-exposed 15 37
without silicosis

most extensive 128 116

disease
 Prevention & management

 Once a diagnosis of silicosis is made the worker

should be removed from further silica exposure.
 Clinical suspicion of the development of
mycobacterial infection must be high.
 Standard tuberculosis treatment regimens are
effective.
 Prevention & management

 Corticosteroid therapy : in patients with acute and

chronic forms especially when silicosis is associated
with autoimmune disease.
 Isoniazid prophylaxis is appropriate when
corticosteroid therapy is prescribed.
 Tetrandrine, a plant alkaloid with antioxidant and anti
inflammatory properties ,has been shown to arrest the
progression of silicosis.
 lung transplantation for workers with extensive
silicosis.
Thanks for attention