This document provides information on occupational lung diseases. It begins with a brief history of occupational lung diseases dating back to Roman times. It then defines occupational lung diseases and pneumoconiosis. The document classifies and describes various types of pneumoconiosis including anthracosis, silicosis, asbestosis, and berylliosis. For each type, it discusses associated occupations, pathogenesis, clinical features, diagnosis, and management. The document provides detailed information on the pathogenesis, clinical presentation, radiographic findings, and complications of major occupational lung diseases like silicosis and asbestosis.

1. Occupational Lung Diseases
Dr. Mohammad Rehan

2. CONTENTS
 History
 Definition
 Classification
 Types
 Pathogenesis
 Anthracosis
 Silicosis
 Asbestosis
 Berylliosis
 Byssinosis
 Others
 Preventive
Measures

3. HISTORY
 It is likely that humans have
suffered from occupational lung
diseases since the change from
hunting to agriculture as a means of
providing food.
 In Roman times it was recorded that
mining was a dangerous trade, fit
only for convicts and slaves.
 The first recorded mention of
breathlessness among handlers of
grain was done by Ramazzini, the
father of occupational medicine, in
1713.
Bernardino Ramazzini
(1633 - 1714)

4. HISTORY
 In the eighteenth and early nineteenth centuries, it was
thought that the symptoms from black lung disease were
asthma-related.
 The term "black lung" was coined when medical
professionals discovered the blackening of miners' lungs
in post-mortem.
 The first documented case of an asbestos-related death
was reported in 1906 when the autopsy of an asbestos
worker revealed lung fibrosis.
 In the early twentieth century, it was observed that many
asbestos workers were dying unnaturally young.

5. HISTORY
 In 1924, Nellie Kershaw, an English
textile worker was the first case of
asbestosis to be described in medical
literature.
 Dr.William Edmund Cooke testified in
Kershaw's inquest that "mineral
particles in the lungs originated from
asbestos and were, beyond reasonable
doubt, the primary cause of the fibrosis
of the lungs and therefore of death"
 Berylliosis was described first in
Germany in 1933 and in the USA in
1943.
Nellie Kershaw
(1891 –1924)

6. Definition
 As per International Labour Organization (ILO)
 The term “occupational disease” covers any disease
contracted as a result of an exposure to risk factors
arising from work activity.
 Two main elements are present in the definition of an
occupational disease:
1) The causal relationship between exposure in a
specific working environment or work activity and a
specific disease; and
2) The fact that the disease occurs among a group of
exposed persons with a frequency above the average
morbidity of the rest of the population.

7.  The term pneumoconiosis derives its meaning from
the Greek words: pneuma = air and konis = dust
 The International Labour Organization defines
pneumoconiosis as “the accumulation of dust in the
lungs and the tissue reactions to its presence”.
 Not included in the definition of pneumoconiosis are
conditions such as asthma, chronic obstructive
pulmonary disease (COPD), and hypersensitivity
pneumonitis, in which there is no requirement for dust
to accumulate in the lungs in the long term.

8. Determinants of inhalational exposure
 Particles size of air contaminates
Particles > 10 -15 um diameter do not penetrate beyond the nose
and throat.
 Particles are divided into three size fractions on the basis of their
size character and source .
1.Coarse-mode fraction –particles size of 2.5- 10 um contain
crustal elements such as silica, aluminum, and iron. Mostly deposit
relatively high in the tracheobronchial tree.
2.Fine mode fraction –particle size <2.5 um and carried to the
lower airways and get deposited .Fine particles are created by
burning of fossil fuels or high temperature industrial process,
gases ,fumes.
3. Ultra fine fraction - <0.1 um in size deposit in the lung and
they come in contact with the alveolar walls ,however particles of
this size range may penetrate into the circulation and be carried to
extra pulmonary sites.

10.  In other words
 Pneumoconiosis can be defined as the non-neoplastic
reaction of lungs to inhaled minerals or organic dust
and the resultant alteration in their structure excluding
asthma, bronchitis and emphysema. – Textbook of
Pulmonary Medicine , D Behera

11. CLASSIFICATION
 1) INORGANIC DUSTS
 2) ORGANIC DUSTS

13. Types
 Pneumoconiosis is usually divided into three groups:
 Major pneumoconiosis
 Minor pneumoconiosis
 Benign pneumoconiosis
“ Fibrotic Pneumoconiosis”

14. Types
 Major Pneumoconiosis: Inhalation of some dusts
results in “major fibrosis” of the lungs, which results
in interference of lung architecture or lung function
tests.
 Examples are:
 Silica  silicosis
 Asbestos  asbestosis
 Coal  anthracosis
Healthy lung Silicotic lung

15. Types
 Minor Pneumoconiosis: Inhalation of some dusts
results in “minor fibrosis” of the lungs
 There is minimal fibrosis of the lungs without
interference of lung architecture or lung function tests.
 These dusts include:
 Mica pneumoconiosis
 Koalin (china clay) pneumoconiosis

16. Types
 Benign Pneumoconiosis: There isn't any reaction in
the lungs, but dust deposition casts a shadow in x-ray
of the lung. There is no fibrosis and no disturbance of
lung functions.
 It can result from the inhalation of:
 Iron dust siderosis
 Tin dust stannosis
 Calcium dust chalcosis
 They are characterized by the presence of small
rounded dense opacities on a chest film due to
perivascular collections of dusts.
 The deposits in the lung disappear when exposure is
discontinued.

17. PATHOGENESIS
 For clinical pneumoconiosis to develop, 3 essential
factors are required:
 Exposure to specific substance: coal, appear relatively
inert and may accumulate in considerable amounts with
minimal tissue response; while silica and asbestos,
have potent biologic effects.
 Particles of appropriate size to be retained in lung (1-
5μm)
 Exposure for a sufficient length of time (usually around
10 years)

18. Pathogenesis

19. CLASSIFIED
Fibrotic
( focal nodular ,diffuse fibrosis)
Nonfibrotic
(particle-laden
macrophages,
no fibrosis )
1.silicosis -Nodular fibrosis
2.coal worker pneumoconiosis
3.asbestosis --Diffuse fibrosis
4.berylliosis- Granulomatous
reaction
1.siderosis
2.stannosis
3.baritosis

20. COAL WORKER PNEUMOCONIOSIS/
ANTHRACOSIS

21. ANTHRACOSIS
• Pathologic entity resulting from deposition of coal dust in
the lungs.
• Simple cwp – with prolonged exposure to coal dust for
15 to 20 years ,small rounded opacities develop usually
not associated with pulmonary impairment.
• Complicated cwp – appearance of nodules> 1cm in
diameter on chest radiography usually confined to upper
half of the lungs . And it progresses to PMF that is
accompanied by severe lung deficits causing chronic
bronchitis and COPD .
• When exposure is terminated the simple type will not
progress; PMF type will progress

22. CAPLANS SYNDROME
 coal workers with rheumatoid disease may
develop nodules even after relatively low
exposures to dust.
 The lesions are typically subpleural.
 The lesions may grow rapidly, appear in crops(in
contrast to silicotic/CWP nodules that appears
over a period of time) cavitate and produce a
pneumothorax

23. CLINICAL FEATURES
 SIMPLE CWP- disease state without symptoms or
physical signs.
 Diagnosis is based on radiologic features
 The symptoms of cough and sputum reported by most
coal miners- consequences of dust induced Chronic
Bronchitis
 Breathlessness on effort- caused by associated
chronic airflow limitation/ by the development of PMF
 Respiratory impairment and disability develop as PMF
progresses

25. Anthracosis
Cut section of lungs in anthracosis On histopathological examination

26. Diagnosis and management
 A history of occupational exposure to coal and a chest
radiograph are the fundamental elements in the
diagnosis of CWP. ( CT when chest x-ray is
insensitive)
 Treatment of latent TB infection should be considered
for coal workers who are thought to have had
significant silica dust exposure or who have evidence
of Silicosis
 Smoking cessation counselling
 Management of Chronic Bronchitis and Emphysema

27. Anthracosis
 In a study conducted by National Institute of
Occupational Health in collaboration with the
International Development Research Centre (IDRC),
Canada, (5777 underground coal miners and 1236
surface coal miners)
 revealed that the prevalence of pneumoconiosis
(category 1/1 and more) in underground coal miners
was 2.84% and in the surface coal workers it was
2.10%.
 The overall prevalence of functional abnormalities of
lung in underground coal miners and surface coal
workers was 45.4% and 42.2% respectively.
Source: www.nioh.org

28. Brick-making Sand blasting
SILICOSIS

29. Silicosis
Occupations with exposure to silica dust
 Mining
 Tunnelling
 Quarrying
 Sandblasting
 Ceramics
 Brick-making
 Silica flour
manufacture
 Slate Pencil Industry
 Agate Industry
 Quartz Grinding

30. SILICOSIS
 There are 3 requirements for the diagnosis of
Silicosis:
 1) History of silica exposure sufficient to cause illness
 2) Chest radiographic features consistent with
Silicosis
 3) Absence of other illnesses that mimic Silicosis
 Other chest illness: Rheumatoid nodules, tumor,
infections, other pneumoconiosis, sarcoidosis
 According to NIOH (National Institute of
Occupational Health, New Delhi) about 3 million
people are occupationally exposed to free silica
dust and are at potential risk of developing silicosis.

31.  Clinical forms:
Acute silicosis- it develops with 10 months of silica
exposure
Clinical and pathologic features are similar to
pulmonary alveolar proteinosis .It is a quite severe
form and is progressive despite discontinuation of
exposure.
 Xray - chest - profuse miliary infiltration or
consolidation,
 No silicotic nodules
 HRCT- characteristic pattern-Crazy paving [thickened
intra and interlobar septa producing polygonal shapes
].
 Treatment- whole lung lavage provide symptomatic
relief

32. Clinical features:
 Chronic cough
 Dyspnea (shortness of breath) that worsens with
exertion.
 Fatigue
 Loss of appetite
 Chest pains
 Acute silicosis patients may also have fever and
experience rapid, unintended weight loss.

33. Simple silicosis-develops with long term (15-20
years) less intense exposure, without associated
impairment of lung function
Xray – chest –variably sized ,poorly defined small
nodules predominating in upper lobes .
Calcification of hilar nodes producing characteristic
feature “EGG shell” pattern.
Egg shell pattern

34.  HRCT-numerous small nodules more pronounced
on upper lobes a number of sub pleural location
RCT shows numerous small nodules

35.  Complicated silicosis-nodular form may progress in the
absence of further exposure with coalescence and
formation irregular masses > 1cm in diameter.
 these masses can become quite large and when this
occurs progressive massive fibrosis term is applied.
 Both restrictive and obstructive pattern may be associated
with PMF.
PMF

36. Silicosis
Chest radiography showing Eggshell
calcification
Polarized light microscopy showing
Crystals of silica

37. COMPLICATIONS
SILICOTUBERCULOSIS-silica is cytotoxic to alveolar
macrophages so patients are at increased risk of tuberculosis.
Also infection with atypical mycobacteria and fungus.
Autoimmune disorder- rheumatoid arthritis , scleroderma
malignancy

38. MANAGEMENT AND
CONTROL
 Change in occupation to an environment free of silica
containing dust.
 Lung lavage to remove silica from lung
 Treatment of all forms of Silicosis should be directed towards
control of mycobacterial disease
 All subjects with Silicosis should have a Tuberculin Skin Test
or IFN-gamma release assay
 Smoking Cessation
 Acute and accelerated silicosis- Lung Transplant

39. ASBESTOSIS
 ASBESTOS is a fibrous hydrated Magnesium Silicate
with more than 3000 commercial uses due to its
indestructible nature, fire resistance etc.
 Types:
1) Chrysolite (serpentine)- M.C. used
2) Amphibole( Amosite)- straight fibre
3) Crocidolite- needle shaped long fibre

40. Serpentine
(93% of commercial use)
Amphibole
(7% of commercial use)
Chrysolite
Actinolite, Amosite, Anthophyllite,
Crocidolite, Richterite, Tremolite
ASBESTOSIS

41. ASBESTOSIS
 Significant occupational exposure to asbestos occurs
mainly in
 Asbestos cement factories
 Asbestos textile industry and
 Asbestos mining and milling. Asbestos cement factories
Asbestos textile industry Asbestos mining

42. Asbestos-related diseases
Benign
Pleural diseases
1.plaques
2.diffuse pleural thickening
3.effusion
4.calcification
Parenchymal diseases
1.Asbestosis [parenchymal
fibrosis caused by asbestos
inhalation]
2.Rounded atelectasis
3.Benign fibrotic masses
4.Transpulmonary bands
Malignancy
1.Malignant mesothelioma
2.Bronchogenic carcinoma

43. Asbestos-Related Pleural Abnormalities
 Four types of abnormalities:
 Pleural plaques
 Benign asbestos pleural effusions
 Diffuse pleural thickening
 Pleural disease puts patient at risk for other asbestos related
diseases – 10% get interstitial fibrosis within 10 years
 Mostly asymptomatic, though some can cause dyspnea or
cough
 Latency periods: 10-30 years
(shorter latency is for pleural effusion)
 No specific therapies
 Pleurectomy in severe cases .

44. ASBESTOSIS
 Symptoms
 Average latency period is 20-30 years
 Dyspnoea
 Cough
 Chest pain
 In advanced cases, clubbing of fingers
 At histopathologic analysis, asbestos bodies, which
may consist of a single asbestos fibre surrounded by
a segmented protein-iron coat, can be identified in
intra alveolar macrophages.

45. ASBESTOSIS
Translucent asbestos fiber (straight
arrow) surrounded by a protein-iron coat
and an alveolar macrophage (curved arrow)
Chest x-ray showing Small, irregular oval
opacities Interstitial fibrosis and “Shaggy
heart sign”

46. Chest Radiograph Findings: Asbestos-Related
Pleural Abnormalities
 Pleural plaques
 Areas of pleural thickening
 Sometimes with calcification
 Pleural effusions
 Diffuse pleural thickening
 Lobulated prominence of
pleura adjacent to thoracic margin
 (over ¼ of chest wall)
 Interlobar tissue thickening
 Rounded atelectasis
 Rounded pleural mass
 Bands of lung tissue radiating outwards

47. ROUNDED ATELECTASIS
 Caused by scarring of the visceral and parietal pleura
and the adjacent lung, with the pleural reaction folding
over on itself.
 The pleural surfaces then fuse to one another,
trapping the underlying lung and leading to
atelectasis.
 As a result of this alteration, a mass lesion that mimics
Lung cancer can be seen on PA chest Radiograph
 This lesion is most easily appreciated to be a
PSEUDOTUMOR with the use of CT scanning

48.  HRCT can non invasively demonstrate continuity to
areas of diffuse pleural thickening, evidence of volume
loss in the adjacent lung, or a characteristic comet tail
of vessels and bronchi sweeping into wedge shaped
mass.
 HRCT scans localised most cases of rounded
atelectasis to the lower, posterior portion of lung(right)

50. Parenchymal Asbestosis
 Diffuse interstitial fibrosis with:
 Associated more with crocidolite
 Smokers more prone to disease
 Radiographic changes: >10 years
 Latency period: 20-40 years

51. Lung Carcinoma
 Latency period: 20-30 years
 Bronchogenic Ca: 5x higher incidence in non-smoking
asbestos workers, 90x higher in smoking asbestos workers.
 Adeno Ca is most common.
 Chrysotile highest risk bronchogenic Ca.

52. Malignant Pleural
Mesothelioma
 Tumor arises from the thin pleural membrane
surrounding the lungs
 Rapidly invasive
 Rare, although incidences are increasing
 Long latency period: Usually 30-40 years

53. Chest Radiograph Findings:
Mesothelioma
 Pleural effusions
 Pleural mass
 Diffuse pleural
thickening

54. • Beryllium – is a light weight metal
• Exposure –manufacture of alloys, ceramics, or
high technology electronics , nuclear reactors
• Beryllium may produce
- Acute pneumonitis,
-Chronic granulomatous inflammatory disesase
that is similar to sarcodisis.
- Lung cancer
• Pathogenesis is a result of delayed type
hypersensitivity reaction stimulating proliferation
of T-cells leading to inflammatory ,fibrosis and
granuloma formation.
BERYLLIOSIS

55.  Clinical features- cough , chest pain, arthralgia's
,fatigue and weight loss
 BeLPT[beryllium lymphocyte proliferation test ]-blood is
drawn and in the lab, the WBC are separated from the rest
of the blood cells and then mixed with beryllium solution. If
the immune system is sensitized to beryllium, the cells will
multiply, producing an abnormal BeLPT result.In normal
individuals cells will not multiply.
 Fiberoptic bronchoscopy with transbronchial lung biopsy is
required to make diagnosis of CBD . Biopsy shows
noncaseating granulomas or monocytic infiltration in lung
tissue.

56. MANAGEMENT
 The diagnosis of CBD- based on documented exposure to
Beryllium, evidence of lung disease compatible with the
diagnosis, and a positive BeLPT performed on blood or BAL
fluid.
 Three categories of Be-associated disorders:
1) Be sensitisation-( +ve Blood or BAL BeLPT but negative
biopsy)
2) Subclinical Be-disease-( +ve BeLPT and biopsy but no
clinical or radiological features of
disease)
3) Chronic Berylliosis- (+ve BeLPT and Biopsy with clinical
and radiological evidence of
disease)
 Most imp. – complete cessation of further exposure

57. BYSSINOSIS
 In 1831 Kay described chest
tightness and fever that
commonly occurred on Monday
after workers had been off work
over the weekend. It was
beacause of this observation that
term MONDAY MORNING
FEVER was coined.
 Certain jobs in the textile mills
are associated with a higher risk
for development of Bronchitis.
 Ginning, opening or carding work
carry a higher degree of risk.

58. CLINICAL FEATURES AND RISK
FACTORS
 SOB occurs often on the day back to the work at
textile mill after several days off as on a Monday after
being off over the weekend.
 Workers with a higher grade of symptoms tend to
have a more rapid decline in Pulmonary Function.
 Risk factors include:
1) Length of employment in a cotton mill
2) Level of dust exposure
 Tobacco smoking has been shown to be synergistic
with exposure to cotton dust in producing Chronic
Bronchitis

59. Grading of
Byssinosis(SCHILLING)
 GRADE 0 – No symptoms on day 1 of work
 GRADE ½- Occasional chest tightness or irritation of
respiratory tract on the 1st workday of week.
 GRADE 1- Chest tightness on every 1st day of
workweek
 GRADE 2 - Chest tightness on 1st and other days of
work week
 GRADE 3 - Chest tightness on 1st and other days of
work week and physiological evidence of permanent
disability.

60. PFT Abnormality
 Characteristically Byssinosis is associated with a
reduction in FVC and FEV 1 on the day of return to
work after an absence.
 The degree of reduction in these parameters
increases over the workday.
 This change is generally more severe on the 1st day of
work after an absence then on subsequent days

61. PATHOGENESIS
 The Histopath. of Byssinosis is similar to those of
bronchitis induced by tobacco smoke- with
hyperplasia of mucus glands and infiltration of bronchi
with PMNs.
 Cotton dust also stimulate mast cells and
macrophages, to release molecules that attract
neutrophils.
 New evidence points to a
Lipopolysaccharide(Endotoxin) produced by bacterial
contaminants of cotton as the causative agent of
Byssinosis.
 Byssinosis has elevated serum Histamine levels.

62. TREATMENT AND PREVENTION
 The most important treatment- removal of the
individual from offending work environment.
 Screening PFTs at the workplace is important to
identify susceptible individuals who exhibit airflow
abnormalities.
 Measures have been taken in developed countries to
control cotton dust levels in textile mills( ex. Steam
clean cotton while it is still in the bale)

63. Other occupation lung
disease

65. Preventive measures
 Preventive measures:
 Medical measures
 Engineering measures
 Other measures

66.  Medical measures:
 Pre-placement examination
 Periodical examination
 Medical and health care services
 Notification
 Maintenance and analysis of records
 Health education and counselling
 Practicing good personal hygiene
Preventive measures

67.  Practicing good personal hygiene:
 Washing hands and face before eating, drinking, going to
the toilet, smoking.
 Do not eat, drink, smoke, or apply cosmetics in areas
where silica is being used.
 Wear protective clothes and respiratory protection
(Respirators must fit tightly.)
 Before leaving work, shower and change into clean
clothes. Leave dusty clothes at work.
Preventive measures

68.  Engineering measures
 Design of building
 Conduct air monitoring to measure the workers’
exposure to crystalline silica.
 Minimize exposures by controlling the creation of
airborne particles, for example, use wet drilling, local
exhaust ventilation.
 Personal Protective Equipments: Provide workers with
protective clothes, respiratory protection, and facilities
for washing (showers) and changing.
 Enclosure / isolation
 Environmental monitoring
Preventive measures

69. Prohibit Dry Cutting Promote wet Cutting
Preventive measures

70. Personal Protective Equipments
70PPT-002-01
Tyvek suit Gloves
Goggles
Boots
Respirator
Preventive measures

71. Fume extractor system Labeling of products
Preventive measures

72.  Other measures:
 Legal measures: Measures to minimize dust emissions
and exposure to dust.
 Law compliance mechanisms, including effective
workplace inspection systems
 Cooperation between management and workers and
their representatives
 A mechanism for the collection and analysis of data on
occupational diseases
 Collaboration with social security schemes covering
occupational injuries and diseases
Preventive measures

73. Preventive measures
 Other measures:
 Training of health professionals in occupational
diseases as majority of medical practitioners lack
training in occupational health and consequently lack
the skills to diagnose and prevent occupational
diseases.

74. THANK YOU