Occupational Lung Disease

Question 1

Diseases encompassed

Answer 1

Occupational asthma
COPD

Pneumoconioses (mineral dust)

• Coal Workers’ Lung
• Asbestosis
• Silicosis

Malignant diseases
Lung cancer, Mesothelioma

Question 2

Occupational history

Answer 2

Detailed history of exposure
Type of material
Duration 
Intensity
Temporal relationship to onset of symptoms

Symptoms - Improvement away from workplace

Question 3

Pneumoconioses

Answer 3

Coal-workers’ pneumoconiosis
140 deaths/yr
Geography UK coalfields

Uncomplicated CWP – mild disease

Progressive Massive Fibrosis
Activation of alveolar macrophages
Progressive scarring causing stiff lungs

Question 4

Silicosis

Answer 4

10-20 deaths/yr

Fibrotic lung disease

- Activation of macrophages	
- Restrictive lung function deficit 
- Eggshell calcification of lymph nodes

Risk factor for TB & lung cancer

Question 5

Treatment of Pneumoconioses

Answer 5

Prevent further exposure
Stop smoking
Monitor lung function

Symptomatic treatment
Cough, dyspnoea, cor pulmonale

No cure

Question 6

Asbestos - Benign

Answer 6

Pleural plaques (marker of exposure)
Benign pleural effusion
Pleural thickening & restriction
Asbestosis (fibrosis)

Question 7

Asbestos - Malignant

Answer 7

Lung cancer
In asbestosis RR of lung cancer:
	7x in non-smokers
	93x in smokers
Mesothelioma
Malignancy of pleura and peritoneum
Expected to peak in 2020

Question 8

Diagnosis of 
Occupational Asthma (OA

Answer 8

Occupational asthma that is caused by workplace exposures

OR

Work-aggravated asthma in which pre-existing cases are made worse by factors in the workplace

Question 9

Workplace factors

Answer 9

Recognition of high risk job
Co-workers similarly affected
Recent changes 
Products used, tasks undertaken
Preventative measures
Ventilation, masks etc

Question 10

Importance of Challenge Testing

Answer 10

Confirm diagnosis when new agent blamed

Identify responsible agent when multiple sensitisers in workplace

Confirm diagnosis when history & PEFR records are equivocal

(rarely) to exclude diagnosis in patient who will otherwise lose their job

Question 11

Challenge Testing

Answer 11

Asthma should be stable
Withhold bronchodilators

A placebo exposure day is advisable

Equipment that delivers known concentration of suspected agent

Monitor spirometry for several hours after each increase in exposure dose
May take several days

Question 12

Allergic OA - High Molecular Weight

Answer 12

Proteins, polysaccharides
80-90% cases
Sensitisation with latency period (weeks-years)

IgE-dependent

Skin prick/allergy testing
Flour (bakers)
Animals (farmers)
Latex
Enzymes (eg detergents)

Question 13

Allergic OA - Low Molecular Weight

Answer 13

Mechanism poorly understood
Usually independent of IgE

Limited utility of skin prick/allergy testing
Isocyanates (printing, plastics)
Metals (welders)
Dyes (hairdressers)

Question 14

Irritant-Induced/Non-Allergic Asthma

Answer 14

Direct effect on airways, not immune-mediated, occurs without pre-existing asthma

Acute
Reactive Airways Dysfunction Syndrome (RADS)
Develops within hours of a single, very high exposure to an irritant

Subacute
Insidious onset of asthma symptoms after multiple moderate/high exposure incidents

Question 15

RADS: some causative agents

Answer 15

Caustic vapours	
Ammonia		
Fire/Smoke
Chlorine 
Tear Gas	
Floor Sealants

Question 16

Pollutant

Answer 16

Any substance that contaminates the environment

Question 17

Toxin

Answer 17

A naturally occurring poison produced within living cells or organisms
Botulinum, Ricin, Snake venom

Question 18

Exposure & Toxins

Answer 18

Exposure is a function of:

• Concentration of toxin/pollutant
• Duration
• Intensity (exercise etc)
• Route (skin vs inhaled)
• Metabolism of toxin

Clinical impact varies with individual susceptibility / comorbidity

Question 19

Toxin susceptibility

Answer 19

Genetic factors
eg protective effect of HbS against falciparum malaria

Co-morbidity / underlying diseases that augment clinical impact of toxic load

Environmental factors
Heat waves, cold snaps, smogs

Question 20

Vehicle Exhaust Pollutants

Answer 20

Primary pollutants
From fossil fuel combustion	
Nitrogen oxide
Sulphur dioxide (diesel)
Carbon monoxide
Particulate matter 
Fine particles of soot and metals forming smog

Secondary pollutants
From reactions between pollutants in the astmosphere

Question 21

NO

Answer 21

No effect on lung function in normals
Augments response to inhaled allergens
Increases likelihood that URTI will cause wheezing in children

Question 22

NO2 and infection

Answer 22

87 volunteers
exposure to 1-2 ppm, 2h/d, 3 days
intranasal challenge with influenza A virus on day 2 
91% infection in those exposed to NO2
71% in control subjects

Question 23

Health Effects of Ground Level Ozone

Answer 23

Decrease lung function
pro-inflammatory effects
- Increase cytokines (IL-6, IL-8, GM-CSF)
- neutrophilic bronchitis

Increase response to inhaled allergens
Increase respiratory morbidity

Question 24

Particulate Matter (PM) & Asthma

Answer 24

PM potentiates risk of airborne allergens causing atopic sensitisation

PM affects airway structural elements
Airway cilia
Mucous production
Oxidative stress to cell DNA
Induction of epithelial apoptosis

PM promotes airway inflammation and ↑ IgE production

Question 25

Exposure reduction

Answer 25

Occupational
FFP masks
ventilation

Environmental
Air quality warnings
Remain indoors, close windows
Minimise duration/intensity of outdoor activities
?anti-oxidants