Complexities of occupational and environmental lung diseases, exploring their causes, symptoms, diagnosis, and prevention measures. For more information please contact us: 9779030507.

1. Occupational & Environmental
Lung Diseases

3. Harmful Effects of Inhaled Particles
Determinant Factors
 Biological factors e.g. allergens, pollens
 Chemical factors e.g. gases, quartz
 Physical factors: asbestos fibers
 Total Mass of inhaled dust is important
Spectrum of Environmental Problems
General: Non-specific, skin, eye & systemic
Specific (Occupational): Inorganic & organic dusts
Gaseous pollutants

4. Respiratory Diseases
 General respiratory symptoms – Cough
 Infections – Tuberculosis
 Asthma: Environmental factors, Occupational asthma
 Chronic Obstructive Pulmonary Disease (COPD)
 Pneumoconioses: Silicosis
 Lung cancer
 Interstitial Lung Disease
 Nonspecific respiratory symptoms

5. Systemic Problems
Cardiac
Hypertension – Atherosclerosis
Ischaemic heart disease – heart attacks
Cardiomyopathies
Cerebrovascular
Atherosclerosis – cerebral, cerebrovasc (Strokes)
Cerebellar, cerebral and spinal syndromes, Musculoskeletal
Neuro-psychiatric – Depression and other emotional disturbances
Gastro-intestinal (mostly water-borne)
Parasitic infestations and other Infections
Diarrhoeas, Dysenteries, Hepatitis, Dyspepsia – ulcers
Cancers

6. Clinical & Aetiological Classification
 Inhalable dust diseases
Deposition: Solid , inorganic dusts
Hypersensitivity: Organic dusts
Hypersensitivity pneumonias
Occupational asthma
 Gases and fumes
 Miscellaneous: Infections, allergies

7. Inorganic Dust Exposures (Occupational)
 Silicosis
 Anthracosis- Coal workers’ pneumoconioses
 Asbestosis
 Deposition of tin, mica

8. Silicosis
 Most prevalent chronic occupational lung disease*
 Irreversible and chronic fibrotic disease caused by
inhalation, retention and pulmonary reaction to large
amounts of silica dust (SiO2)
 Mining, stone cutting, ceramic, pottery, agate, brick
making, slate pencil, etc. are a few of the many industries
which are particularly at risk

9. Clinical Course – 3 forms
 Chronic/Classic Silicosis
 Accelerated Silicosis
 Acute Silicosis

10. Chronic Silicosis
 Develops following low-to-moderate level exposure to silica dust for
>20 yrs
 1st  Silica laden macrophages accumulate
 Later  Silicotic nodules form as a result of host response to the
foreign body
 Nodules mainly seen in upper lobes
 Calcified LN maybe seen
 Nodules enlarge and coalesce (>2cm)  PMF or complicated
silicosis
 Increased susceptibility to TB and cavitation

13. Accelerated Silicosis:
 Heavy silica exposure in <5-10 yrs
 Progresses faster than chronic silicosis
 Sometimes associated with CTD
Acute silicosis
 V.High concentration of silica exposure over weeks to months – eg.
Sandblasters, rock drilling, etc
 B/l alveolar opacities without silicotic nodules
 Intense inflammatory reaction due to freshly fractured silica particles
 Hypertrophic Type II pneumocytes  produce excess surfactant 
Resembles PAP

14. Complications
 Tuberculosis
 Cor pulmonale
 Spontaneous pneumothorax
 Broncholithiasis
 Tracheobronchial obstruction
 Lung cancer
 Hypoxemic ventilatory failure

15. Silico-tuberculosis
 The association of Silicosis and TB has been suspected
several hundred years
 Exposure to silica causes a renewed multiplication of
bacilli in the healing TB lesions
 Increased risk of PTB in silicosis
 Exposure of silica has an unfavourable influence on the
course of induced TB

16. Interaction of silicosis with TB
 There is more fibrosis produced by combination
 Synergistic effect of silicosis and TB – proliferative
fibrous reaction  Rapid fibrosis
 TB may complicate simple silicosis as well as advanced
disease
 It may develop PMF with cavitation
 Poor response to ATT Longer duration needed

17. Treatment of Silicosis
 No specific therapy for silicosis
 Prevent further exposure to silica dust
 Strongly advise patients to quit smoking
 Immunize against influenza, pneumococci
 Experimental approaches tried without success are - whole-lung
lavage, aluminum inhalation, and corticosteroids
 Screen for TB with sputum AFB x 2
 Complications should be treated appropriately

18. Prevention
 Dust suppression,
 Process isolation,
 Ventilation,
 Use of non–silica–containing abrasives.
 Respiratory masks
 Surveillance of exposed workers with respiratory
questionnaires, spirometry, and chest x-rays is
recommended

19. Diseases associated with exposure to Silica
dust
 Occupational asthma
 Chronic obstructive pulmonary disease
◦ Emphysema
◦ Chronic bronchitis
 Mineral dust induced small airway disease
 Lung cancer
 Mycobacterial infection
◦ MTB
◦ NTM
 Immune –Related Disease
◦ PSS, RA, CRD, SLE

20. Coal Workers Pneumoconiosis
 Coal dust consists of carbon (60-80%), apart from 50 different
elements and oxides – including Silica
 Higher the quality of coal – higher the silica content in the dust
 2 forms: simple CWP and PMF
 Three Criteria needed for diagnosis of CWP:
◦ CXR consistent with CWP
◦ A work history sufficient in exposure and latency to cause CWP
◦ Absence of other illnesses which mimic CWP

21. Simple CWP
 Small rounded opacities – from pinhead sized to 1 cm
 1st upper zones  then all over lung fields
 Slowly progressive illness over decades
 Chest radiograph correlates with amount of coal dust inhaled
 Pathology: Coal macule is characteristic lesion
 Consists of coal dust, reticulin fibres and coal laden macrophages
 Later enlarges and forms coal nodule
 Surrounded by focal area of emphysema
 Silicotic nodules may coexist

22. PMF: Progressive Massive Fibrosis
 When one or more nodules attain a size of >2cm
 MC in posterior segments of upper lobes or superior
segments of lower lobes
 Assymetrical
 Development influenced by:
◦ Combined inhalation of silica
◦ NTM infection
◦ Immunologic response

23. Other diseases caused by coal
 COPD
 Industrial bronchitis
 Caplan’s syndrome
Complications:
 Cor pulmonale
 Pneumothorax
 Hypoxemic Respiratory failure
 Silicotuberculosis more common when exposed to high levels of
silica in coal dust

24. Asbestosis
 Asbestosis highly dangerous, but extremely useful
industrial material.
 Used in cement, building material, plastic, insulation,
fire proofing, ship building, Railway workshops,
cement & friction product manufacture
 Environmental pollution is known.

25. Asbestosis
 Exposure to asbestos causes: asbestosis, lung cancer,
mesothelioma of pleura and peritoneum , Interstitial
lung fibrosis
 Asbestos fibres are fire-resistant, indestructible. An
inhaled fibre may lie dormant for several years to cause
lung damage

26. OTHER DEPOSITION DISEASES
 Other silicate materials: Talc, Kaolin, Mica, Cement
Erionite (Fibrous aluminium silicate)
Man made vitreous fibres e.g.
Glass wool, rock wool, ceramic fibres
 Siderosis, Stannosis, Baritosis,
 Tungston, Carbon, Antimony
 Produce X-ray abnormalities, but no functional change
 Minimal inflammatory response

27. ORGANIC DUST DISEASES
Occupational Asthma
Hypersensitivity Pneumonias (HP)
Farmer’s Lung: Agricultural exposures, fungi.
Byssinosis: Cotton, Textile, Jute Industry
‘Monday morning illness’, ‘Acute Mill Fever’,
‘weavers’ cough. 7-9% in Textile workers
Prevention: dust levels < 0.5 mg/m3
Drugs and chemicals

28. Hypersensitivity Pneumonias
 Type 3 immunological response to sensitizing antigens (Cf. type 1 for
asthma)
 Presentation delayed 4-6 hrs or more after exposure
 Symptoms: Cough, fever, breathlessness, malaise etc
 Types: Farmer’s lung, Byssinosis, Baggasosis
Psittacosis, Pigeon breeder lung, Grain lung,
Air-conditioner lung, compost lung etc
Diagnosis: History of exposure-symptom relationship
CXR; Non-specific. Eosinophilia, Antibodies
Tmt: Removal of offending antigens
Symptomatic and anti-inflammatory treatment

29. Byssinosis
 Byssinosis is an occupational lung disease caused by exposure
to cotton, flax and hemp dust.
 Presents with asthma-like symptoms
 Maximum number of workers with byssinosis are reported in
the cotton textile industry as it is one of the largest industries
in the world.
 The workers engaged in the initial processes of textile
manufacturing (blow, card, frame and ring frame) are exposed
to cotton dust and develop the disease after some years of
exposure.

30. Other environmental exposures
Gases & Fumes
Accidental leakage:
Bhopal tragedy (MIC)
Occupational.
Mechanisms
Asphyxiation – CO2,
Nitrogen, Methane
Irritation: NH3, Chlorine,
SO2,O3, Phosgene
Infections
Respiratory tract
Infections & Pneumonias
Tuberculosis
HIV
Anthrax
Parasitic
Viral

31. Effects attributed to long term exposure
 Mortality due to cardiovascular and respiratory disease
 Chronic respiratory disease incidence and prevalence (asthma,
COPD, chronic pathological changes)
 Chronic changes in physiologic functions
 Lung cancer
 Chronic cardiovascular disease
 Intrauterine growth restriction (low birth weight at term,
intrauterine growth retardation, small for gestational age

32. Other Indoor pollution
Aero-allergens:
Sources- Dampness, Pets
Poor ventilation
 Thermophilic actinomycetes
 Fungi, Aspergillosis, Bacteria
 Other sensitizing antigens
Humidity: Low relative humidity
Dryness of eyes & respiratory tract
Electromagnetic hypersensitivity:
Deleterious effects in patients with asthma, diabetes, multiple
sclerosis,fatigue, fibromyalgia

33. Exposure Antigens Diseases
Mouldy hay6 Thermophilic actinomycetes Farmer’s lung
Mouldy bagasse7
Thermophilic actinomycetes Bagassosis
Mouldy compost and mushroom8
Thermophilic actinomycetes Mushroom worker’s disease
Contaminated barley9
Aspergillus clavatus Malt worker’s lung
Compost10
Aspergillus spp. Compost lung
Esparto grass11
Aspergillus spp. Esparto dust lung
Soy sauce brewing12
Aspergillus spp. Soy sauce lung
Contaminated humidifiers, air Thermophilic actinomycetes Ventilator lung
conditioners, heating systems13
Domestic birds14
Bird proteins Bird fancier’s lung
Pigeon droppings15
Serum, feathers, droppings Pigeon breeder’s disease
Parakeets16
Serum, feathers, droppings Budgerigar fancier’s lung
Silkworm larvae17
Silkworm larvae proteins Sericulturist’s lung
Grains18
Grain weevil Grain lung
Isocyanates19
Altered proteins Hypersensitivity pneumonitis
Wood cutting20
Plant protein Woodman’s disease
Contaminated metal working fluid21
Pseudomonas spp Machine operator’s lung
Detergent enzymes22 Bacillus subtilis Detergent worker’s disease
(washing powder lung)
Contaminated basement23
Cladosporium spp, Penicillium spp Basement lung
Contaminated hot tub water24
Mycobacterium avium complex Hot-tub lung
House dust25 Trichosporum asahii Japanese summer house hypersensitivity
pneumonitis

34. Occupational Asthma
 Animal proteins
 Plant proteins
 Legumes and seeds
 Wood dusts
 Antibiotics and other drugs manufacturing
 Metal salts- platinum, cobalt, nickel, chromium
 Diisocyanates
 Dyes and chemicals

35. Diagnosis & Treatment
 Exposure-symptom relationship
 Radiological investigations
 Immunological investigations: Skin test, antibody
demonstration
 Occasionally, histopathology
Management: Largely symptomatic
Reduction/ removal of exposure
Management of complications