SILICOSIS - Silicosis is caused by inhalation of crystalline silica particles between 0.5-5.0 μm in diameter over prolonged periods. - It can manifest as simple silicosis with nodular lesions seen on x-ray or progress to progressive massive fibrosis (PMF) with severe lung impairment. - Accelerated or acute silicosis occurs after short but high levels of exposure and rapidly progresses to PMF and respiratory failure within a few years.

1. SILICOSIS
S I L I C O S I SBy Drx Jayesh mohansing rajput,
jess college of pharmacy, nandurbar, maharashtra

4. •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.
•Between 1968 and 1990 there were 13,744 deaths in
the US where the death certificate mentioned silicosis.

5. OSHA permissible exposure limit (PEL) is 100 μg/m3
for an 8-hour work exposure.
Bronchitis, a well-recognized effect of chronic dust
inhalation, can occur with silica dust inhalation.
Silica exposure can be associated with:
1.Autoimmune diseases :
2.Nephropathy
3.Tuberculosis
4.lung cancer
Scleroderma
SLE
RA

6. SILICA
(silicon dioxide)
FREE : 1.quartz (including granite)
2.flint
3.opal
4.diatomite.
Combined (silicates) :1.asbestos
2.talc
3.kaolin

7. Asbestos
Mg3Si2O5(OH)4

10. Kaolin : Al2Si2O5(OH)4

11. SILICA
Crystalline form: 1. quartz (in sand and many rocks)
2.Cristobalite
3.Tridymite
4.Coesite
5.Shistovite
naturally in lava and
formed by the heating
of quartz or amorphous
silica.
Amorphous
Crystalline form silica are different in their structure, fibrogenicity,
and biologic activity.
Amorphous silica is relatively less fibrogenic and does not cause
lung fibrosis.
1.Diatomite (skeletons of marine organisms)
2.Vitreous silica (glass)

17. Major industries with silica exposure

23. 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
government standards.
Some workers developing much more severe disease
than others.
Most forms of silicosis develop slowly. Usually 10 to
30 years are required from the beginning of exposure
to the onset of clinical manifestations.

24. 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.

25. Classification of silicosis
Simple
- classic
PMF
- accelerated
- acute
SILICOSIS
Miner's lung with silicosis

26. 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.

27. 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.
CLASSIC SILICOSIS

28. Diagnosis
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
There are three requirements for the diagnosis of
silicosis:

29. 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.

30. 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

31. 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.

33. 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.

36. 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.

37. Hilar lymph nodes are often enlarged with a
distinctive peripheral calcification, described
as eggshell calcification.

40. 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.

41. 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

42. 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.

43. 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.

44. 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

48. 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.

49. Chest radiograph from a 56 year-old man taken 7
years after ceasing employment at a silica flour mill
where he had been employed for 6 years as a bagger.
He complained of symptoms of dyspnea and chronic
bronchitis.
He had an 8-year smoking history. Spirometry showed
borderline restriction. The chest radiograph showed
profuse small rounded opacities and progressive
massive fibrotic lesions in the right upper and mid-
zones.
Case 1

51. CX-Ray from a
surface mine driller.
smoked heavily for
many years.
Asymmetric bilateral
upper zone progres -
sive massive fibrotic
lesions are present.
larger and denser left-
sided mass lesion
raises concern of a
pulmonary maligna-
ncy.
Case 2

52. Chest radiograph from a worker employed for many
years in a glass factory with silicosis who then
experienced a relatively aggressive downhill course.
 Investigation revealed infection with M. tuberculosis.
Although he responded to multiple drug therapy, he still
had severe progressive massive fibrosis, extensive
emphysema, and impaired function.
Case 3

54. 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.
Accelerated silicosis

55.  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

56. Initial
Exposure
•Cough
•Weight loss
•Fatigue
•Pleuretic pain
•Crackles
•Cyanosis
•Cor pulmonale
•Respiratory failure
1-3 years 1 year
Death
Acute silicosis
symptoms occurring less than a year after beginning sandblasting have been
reported.

57. ASSOCIATED ILLNESSES
• Mycobacterial infections
• Carcinoma of the lung
• Connective tissue disease
• Renal and extra pulmonary involvement

58.  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

59. 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

60.  The combination of silicosis and tuberculosis is more
difficult to treat.
 Those with silicosis should undergo regular PPD skin
testing.
Mycobacterial infection

61. 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 .

62. (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.
Carcinoma of lung

63. 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.
Connective tissue disease

64. • 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 )
Renal & extra pulmonary involvement

65. 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

66. Medical screening of silica-exposed
workers is generally recommended,
using
questionnaires
chest x-rays
spirometry.
And….PPD
Prevention & management

67. 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

68. The rate of FEV1 and FVC decline increased
with profusion of opacities.
According to one study:
Decline in FEV1 at
year
Decline in FEC at
year
silica-exposed
without silicosis
15 37
most extensive
disease
128 116
Prevention & management

69. 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

70. 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.
Prevention & management

72. Thanks for your attention