Pneumoconiosis- dust with size and different types of occupational pneumoconic diseases, clinical features, diagnosis and prevention of pneumoconiosis.

1. Dr. Sravani
Assistant Professor

2. Definitions
• 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.

3. Dust within the size range of 0.5mm to 3 micron, is health hazard
producing, after a variable period of exposure, a lung disease known as
PNEUMOCONIOSIS, which may gradually cripple a man by reducing
his working capacity due to lung fibrosis and other complications.

4. INHALATION:
• Dust is finely divided solid particles
• Dust ranges from 0.5 – 150 microns
• Released into atmosphere during crushing, grinding, abrading,
loading and unloading.
• >10 microns – settle down
• <5 microns – inhaled
• Ogranic & inorganic
• Soluble & insoluble

5. The hazardous effects of dusts on the lungs depend upon a number of
factors such as:
a. Chemical composition
b. Fineness
c. Concentration of dust in the air
d. Period of exposure
e. Health status of the person exposed.

6. Definitions
• 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

7. 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)

8. Pathogenesis
• From an occupational health point of view, dust is classified by
size into following categories:
• Inhalable Dust: is the one which enters the body, but is trapped
in the nose, throat, and upper respiratory tract. Particle size is
usually 6-25μm.
• Respirable Dust: particles that are small enough to penetrate
the nose and upper respiratory system beyond the body's
natural clearance mechanisms of cilia and mucous and are
more likely to be retained in the lungs. Particle size is usually
1-5μm.
• Particles of <1 μm are exhaled out.

9. Pathogenesis

10. Pathogenesis

11. FIBROSIS
Pulmonary Fibrosis is a chronic lung disease that causes
inflammation, scarring, thickening and stiffening of the lung’s
tissues.

13. Types
– Silicosis – from silica dust
– Asbestosis – from asbestos dust
– Coal workers pneumoconiosis (anthracosis) – from coal
dust
– Byssinosis – from cotton dust
– Bagassosis – from sugarcane dust
– Farmer's lung - from hay
other agricultural products.
– Berylliosis – from beryllium
dust or mold spores or

14. Types
– Siderosis – from iron oxide
– Tanosis – from tin oxide
– Talcosis – from talc (hydrated magnesium silicate)
– Bauxite fibrosis – from bauxite dust
– Mixed dust pneumoconiosis – from a mixture of dusts
– Hard metal pneumoconiosis – from certain metals like
cobalt.
– In addition, others dust such as aluminum, barium,
antimony, graphite and mica can also cause
pneumoconiosis

15. Types
• Pneumoconiosis is usually divided into three groups:
– Major pneumoconiosis
– Minor pneumoconiosis
– Benign pneumoconiosis
“ Fibrotic Pneumoconiosis”

16. 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

17. 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

18. 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 Tannosis
– 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.

19. Silicosis
• Develops with repeated and usually long-term exposure to
crystalline silica (silica dust)
• The silica dust causes irritation and inflammation of the
airways and lung tissue.
• Scar tissue forms when the inflammation heals, resulting in
fibrosis that gradually overtakes healthy lung tissue.
• The fibrosis continues extending through the lungs even after
exposure ends.

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

21. silicosis
Brick-making Sand blasting

22. silicosis
Exposure:
• Incubation period vary from few months to 6 years of
exposure.

23. Silicosis
CLINICAL FEATURES:
• Chronic cough
• Dyspnea (shortness of breath) that worsens with exertion.
• Fatigue
• Loss of appetite
• Chest pain
• Acute silicosis patients may also have fever and experience
rapid, unintended weight loss.

24. Phagocytes Ingest dust Accumulate block LC
Pathologically, Dense “nodular” fibrosis.
Nodules: 3 – 4 mm in diameter.
Advanced cases, Impairement of TLC.
X-ray Findings show: ‘Snow-storm’ appearance.

25. Silico-tuberculosis
• Pulmonary tuberculosis occurs in about 25% of patients with acute
or classic silicosis.
• "Eggshell" calcification, when present,is strongly suggestiveof
silicosis
• On histopathology, the hallmark of silicosis is the silicotic nodule

26. silicosis
Chest radiography showing Eggshell
calcification
Polarized light microscopy showing
Crystals of silica

28. Prevention
Dust Control Measures:
• Substitution,
• Complete enclosure,
• Isolation,
• Hydroblasting,
• Good house-keeping,
• PPE or measures
Regular physical examination

29. ASBESTOSIS
• Asbestosis is diffuse interstitial pulmonary fibrosis that occurs
secondary to the inhalation of asbestos fibers.
• It is considered separately from other asbestos-related
diseases, such as benign pleural effusion, plaques, malignant
mesothelioma, and bronchogenic carcinoma.

30. • They are silicates of varying composition.
• Silica combined with bases of magnesium, Fe, Ca, Na and Al.

31. Serpentine
(93% of commercial use)
Amphibole
(7% of commercial use)
Chrysolite Amosite,Crocidolite,
ASBESTOSIS
Anthophyllite,

32. Serpentine- Hydrated magnesium silicate
Asbestos fibres are 20 – 500 microns in length and 0.5 – 50
microns in diameter.

33. 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

34. ASBESTOSIS
• Symptoms
– Average latency period is 20-30 years
– Dyspnoea
– Cough
– Chest pain
– In advanced cases, clubbing of fingers, cardiac distress and
cyanosis.
• At histopathologic analysis, asbestos bodies, which may
consist of a single asbestos fiber surrounded by a segmented
protein-iron coat, can be identified in intraalveolar
macrophages.

35. • The fibrosis is due to mechanical irritation, peri- bronchial and
diffuse in character.
• Basal in location.
• Sputum shows “ Asbestos bodies ”

36. 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”

37. ASBESTOSIS
• Treatment Strategy:
– Stopping additional exposure
– Careful monitoring to facilitate early diagnosis
– Smoking cessation
– Regular influenza and pneumococcal vaccines
– Disability assessment
– Pulmonary rehabilitation as needed
– Aggressive treatment of respiratory infections
– Health education to patient

38. Anthracosis
• Anthracosis/ Coal Worker's Pneumoconiosis (CWP) / Black
lung disease:
– Accumulation of coal dust in the lungs and the tissue's
reaction to its presence.
– Associated with coal mining industry
– Takes one or two decades to cause symptoms
– The disease is divided into 2 categories:
• Simple Pneumoconiosis
• Progressive Massive Fibrosis (PMF).

39. Anthracosis
• Simple Coal Worker's Pneumoconiosis:
– Said to exist in the presence of radiological opacities < 1cm
in diameter.
– Benign disease if no complications.
– Common symptoms: cough, expectoration (black in colour)
and dyspnea.
– Slight decrease in FVC and FEV1/FVC

40. Anthracosis
• Complicated Coal Worker's Pneumoconiosis
– Is diagnosed when large opacity of 1cm or more in
diameter is observed in the CXR
– Pathologically it is characterized by large masses of black
colored fibrous tissue.
– Symptoms are similar but more severe
– Recurrent pulmonary infection
– The large lesions may cavitate as a result of ischemic
necrosis or infection (T.B).
– PFT (Pulmonary function test) reveals decreased FVC,
FEV1/FVC and increased residual volume.

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

42. Byssinosis
• Byssinosis:
– Caused by inhalation of cotton fibre dust (textile and fibre
industries)
– The chief symptoms are
• Chest tightness
• Shortness of breath
• Cough and
• Wheezing
– Typically occurring when patients return to work after a
weekend or vacation.
– Smoking significantly exacerbates byssinosis

43. Byssinosis
• When detected in its early stages (acute byssinosis), byssinosis
is reversible by eliminating exposure to the responsible irritant.
• When exposure continues the byssinosis can cause permanent
damage to the lungs (chronic byssinosis)

44. • Treatment:
• In the acute setting, patients are encouraged to consider alternative
occupations or at least reduce the exposure in the work
environment.
• Smokers should be encouraged to stop smoking.
• In the acute stages, treatment may include :
1. Brochodilators for symptomatic relief
2. Corticosteroids are best avoided for as long as possible, given
only in severe cases

45. Chronic byssinosis:
• Supportive measures
1. Nebulizer use
2. Home oxygen therapy
• Physical activity and breathing exercises may help in
the management.

46. Bagassosis
Inhalation of bagasse or sugarcane dust.
Sugar-cane earlier went to waste, now utilized in paper, cardboard and
rayon manufacture.
Due to thermophilic actinomycete - Thermoactinomyces sacchari
Symptoms:Breathlessness, cough, haemoptysis and slight fever.
Initially- acute diffuse broncolitis
Skiagram – Mottling in lungs or shadow.

47. Pulmonary Impairment.
If treated early, resolution of acute inflammatory condition of lung.
Untreated, diffuse fibrosis, emphysema and bronchiectasis.

48. Prevention
1. Dust Control
2. Personal Protection
3. Medical Control
4. Bagasse Control

49. Farmer’s Lung
Inhalation of mouldy hay or grain dust.
>30% moisture content – bacteria and fungi grow rapidly
rise of temperature to 40-50 degree C
Thermophilic actinomycetes
(Micropolyspora faeni)

50. • 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

51. • 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

52. Prohibit Dry Cutting Promote wet Cutting
Preventive measures

53. Personal Protective Equipments
52
Tyvek suit Gloves
Goggles
Boots
Respirator
Preventive measures

54. Fume extractor system Labeling of products
Preventive measures

55. 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.