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2. Occupational lung diseases
Ali naserbakht , MD
مرکز تخصصی پایش طب کار البرز

3. INHALATION EXPOSURE Airways Bronchioles Alveoli Interstitium Blood
Systemic
effects
paraquat

4. Site & intensity of the injury
Physico-chemical properties
Particle size…<5u go deeper
Concentration…
Solubility
Density… lighter (as) go deeper
Reactivity… higher (NH4) more damage
Duration of exposure
Rate / depth of breathing
Host response variability / susceptibility
Host defense mechanisms

5. Site of respiratory tract deposition
Water solubility
examples
Site of injury
High
Moderate
low
Ammonia
Chlorine
Nitrogen dioxide
Upper airway
Lower airway
Lung paranchyma
Particle size
>10µm
2. 5-6µm
<2.5µm
Dust from earth crust
Some fire smoke particles
Metal fume, asbestos fiber

6. Mechanisms Irritant : chemicals Allergic : flour (bakers)
fibrogenic : silicosis
Carcinogenic uranium,asbestosis

7. local systemic BRONCHITIS ASTHMA PULM EDEMA PNEUMONITIS FIBROSIS
AIRWAYS
BRONCHITIS
ASTHMA
local
PULM EDEMA
PNEUMONITIS
FIBROSIS
EXPOSURE
ALVEOLI
SYSTEMIC
systemic
NEUROTOXINS
FEVERS

8. Evaluation of patient History Physical exam Imaging studies
Pulmonary function testing

9. Symptoms Cough Hemoptysis Dyspnea at rest and/or on exertion Wheezing
Chest tightness / pain
Upper airways symptoms
Fever, chills

10. Pulmonary function test
Spirometry values:
FVC(FEV6): forced vital capacity - total amount air exhaled
FEV1: amount of air exhaled during the first second of forced expiration
FEV1/FVC% :The ratio of FEV1 to FVC, expressed as a percentage

11. Interpretation
Normal: both the FVC and the FEV1/VC ratio are normal.FEV1& FVC≥ FEV1/VC ≥ 70
Obstructive: FEV1/FVC ratio is below the normal range.
Restrictive: reduction in the FVC without reduction of the FEV1/FVC ratio. This is most reliably interpreted on the basis of TLC.

12. Toxic inhalation injury
Irritation
Inflammetion
Decreased mucociliary clearance
Edema
Asphyxiation

13. Simple
Carbomonoxide-fires
Methane, CO2-manure pits
Chemical
H cyanide-burning plastics
H sulfide-manure pits

14. Occupational diseases
Asthma
Bronchitis
Silicosis
HP,MMF
Acute
Chronic
Progressive
Regressive
Intermitent
Reversible
Irreversible

15. Occupational Asthma Types of Work-Related Asthma :
Work-aggravated asthma
Reactive airway dysfunction syndrome (RADS)
Allergic occupational asthma

16. Definition Occupational asthma
Diagnosed Asthma
Onset after entering workplace
C. Association of symptoms to workplace
D1. Agent known to cause OA or
D2. Work-related changes in lung function

17. Agents of Reactive Airway Dysfunction Syndrome
Hydrochloric acid
Hydrogen sulfide
Locomotive/diesel exhaust
Phosgene
Phosphoric acid
Sodium hydroxide
Sulfuric acid
Tear gas
Toluene diisocyanate
Welding fumes
Zinc chloride

18. Agents of Allergic Occupational Asthma
High-molecular-weight substances
Animal & and plant proteines
Latex
Grain dusts
low-molecular-weight substances
Diisocyanates
Colophony
Western red cedar
Metals (chromium, platinum, nickel)
Glutaraldehyde, formaldehyde

20. Hypersensitivity pneumonitis
Lung disease resulting from sensitization and recurrent exposures to organic dusts
Symptoms: HP presents acutely, as flu-like illness with cough; subacutely, as recurrent "pneumonia"; and chronically, as exertional dyspnea, productive cough and weight loss.
Latency: few weeks to years;
Onset of symptoms after acute exposure: 4 to 12 hours
Repeated exposure to: 1) bioaerosols of microbial or animal antigens; or 2) a few reactive chemicals

21. Hypersensitivity Pneumonitis
Microbial
Bacteria
Thermophiles
NonThermophiles
P. fluorescens
B. cereus, B subtilis
Fungi :
Aspergillus sp,Penicillium,
Amebae
Mycobacteria avium
Animal
Birds, rats
dander,feathers, droppings, urine
Insects:weevil
Chemicals
Metal fluid
Diisocyanates
Pyrethrum

22. PROGNOSIS- OUTCOME Treatment Resolve
Recurrent disease= outcome determinant
Fibrosis / COPD
Fatal,progressive
Treatment
Avoidance of exposure
Corticosteroids

23. Inhalation fever Metal fumes, polymer fumes Contaminated water sources
Contaminated agricultural dusts

24. pneumoconiosis A type of O-ILDs.
Due to inhalation and deposition of mineral dust within lung parenchyma.
Induce tissue reaction
May cause disruption of alveolar architecture or collagen fibrosis.

25. Common features of all pneumoconiosis
Deposition of mineral dusts in lung tissue.
Presence of parenchymaL tissue reaction
Positive chest x-ray findings

26. Silicosis
A collagenous pneumoconiosis caused by inhalation of respirable (0.2 – 10 µm ) free crystalline silicon dioxide ( SiO2 ).
Chronic diffuse interstitial fibro nodular lung disease.
High-dose and long-time inhalation is required.

27. Silica exposure
Minning
Foundry work
Sand blasting
Ceramics
HOST

28. Silicosis
Calcified lymph nodes
Upper lobe nodules

29. Silicosis

30. Asbestosis

31. Products that can contain asbestos
Pipe covering
Asbestos cloth
Cements
Roofing materials

32. Asbestos related lung disease
Clinical presentation: exertional dyspnea,, cough, chest pain, clubbing
• X Ray: reticular veiling lower lobes, ground glass
pleural changes, PMF in mixed exposure,
• Lung fx: restrictive, diffusion↓, art hypoxemia,

33. Coal worker pneumoconiosis
Coal worker's pneumoconiosis (CWP) can be defined as the accumulation of coal dust in the lungs and the tissue's reaction to its presence:
simple CWP (SCWP)
pulmonary massive fibrosis (PMF)

34. Coal workers pneumoconiosis
Radiology: nodular veiling upper lung
zones, nodules > 1 cm indicative of PMF
• Lungfx: normal – simple type
restrictive – complicated type
• Prognosis: simple type – good
complicated type – cardio-respiratory
failure

35. Coal worker pneumoconiosis

36. OCCUPATIONAL LUNG
DISEASES ARE
PREVENTABLE

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39. Complex exposures